---
_id: '15151'
abstract:
- lang: eng
  text: Eukaryotic DNA-binding proteins operate in the context of chromatin, where
    nucleosomes are the elementary building blocks. Nucleosomal DNA is wrapped around
    a histone core, thereby rendering a large fraction of the DNA surface inaccessible
    to DNA-binding proteins. Nevertheless, first responders in DNA repair and sequence-specific
    transcription factors bind DNA target sites obstructed by chromatin. While early
    studies examined protein binding to histone-free DNA, it is only now beginning
    to emerge how DNA sequences are interrogated on nucleosomes. These readout strategies
    range from the release of nucleosomal DNA from histones, to rotational/translation
    register shifts of the DNA motif, and nucleosome-specific DNA binding modes that
    differ from those observed on naked DNA. Since DNA motif engagement on nucleosomes
    strongly depends on position and orientation, we argue that motif location and
    nucleosome positioning co-determine protein access to DNA in transcription and
    DNA repair.
article_processing_charge: No
article_type: review
author:
- first_name: Alicia
  full_name: Michael, Alicia
  id: 6437c950-2a03-11ee-914d-d6476dd7b75c
  last_name: Michael
  orcid: 0000-0002-6080-839X
- first_name: Nicolas H.
  full_name: Thomä, Nicolas H.
  last_name: Thomä
citation:
  ama: Michael AK, Thomä NH. Reading the chromatinized genome. <i>Cell</i>. 2021;184(14):3599-3611.
    doi:<a href="https://doi.org/10.1016/j.cell.2021.05.029">10.1016/j.cell.2021.05.029</a>
  apa: Michael, A. K., &#38; Thomä, N. H. (2021). Reading the chromatinized genome.
    <i>Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.cell.2021.05.029">https://doi.org/10.1016/j.cell.2021.05.029</a>
  chicago: Michael, Alicia K., and Nicolas H. Thomä. “Reading the Chromatinized Genome.”
    <i>Cell</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.cell.2021.05.029">https://doi.org/10.1016/j.cell.2021.05.029</a>.
  ieee: A. K. Michael and N. H. Thomä, “Reading the chromatinized genome,” <i>Cell</i>,
    vol. 184, no. 14. Elsevier, pp. 3599–3611, 2021.
  ista: Michael AK, Thomä NH. 2021. Reading the chromatinized genome. Cell. 184(14),
    3599–3611.
  mla: Michael, Alicia K., and Nicolas H. Thomä. “Reading the Chromatinized Genome.”
    <i>Cell</i>, vol. 184, no. 14, Elsevier, 2021, pp. 3599–611, doi:<a href="https://doi.org/10.1016/j.cell.2021.05.029">10.1016/j.cell.2021.05.029</a>.
  short: A.K. Michael, N.H. Thomä, Cell 184 (2021) 3599–3611.
date_created: 2024-03-21T07:54:19Z
date_published: 2021-07-08T00:00:00Z
date_updated: 2024-03-25T12:31:39Z
day: '08'
doi: 10.1016/j.cell.2021.05.029
extern: '1'
intvolume: '       184'
issue: '14'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.cell.2021.05.029
month: '07'
oa: 1
oa_version: Published Version
page: 3599-3611
publication: Cell
publication_identifier:
  issn:
  - 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Reading the chromatinized genome
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 184
year: '2021'
...
---
_id: '15262'
abstract:
- lang: eng
  text: The Hunchback (Hb) transcription factor is crucial for anterior-posterior
    patterning of the Drosophila embryo. The maternal hb mRNA acts as a paradigm for
    translational regulation due to its repression in the posterior of the embryo.
    However, little is known about the translatability of zygotically transcribed
    hb mRNAs. Here, we adapt the SunTag system, developed for imaging translation
    at single-mRNA resolution in tissue culture cells, to the Drosophila embryo to
    study the translation dynamics of zygotic hb mRNAs. Using single-molecule imaging
    in fixed and live embryos, we provide evidence for translational repression of
    zygotic SunTag-hb mRNAs. Whereas the proportion of SunTag-hb mRNAs translated
    is initially uniform, translation declines from the anterior over time until it
    becomes restricted to a posterior band in the expression domain. We discuss how
    regulated hb mRNA translation may help establish the sharp Hb expression boundary,
    which is a model for precision and noise during developmental patterning. Overall,
    our data show how use of the SunTag method on fixed and live embryos is a powerful
    combination for elucidating spatiotemporal regulation of mRNA translation in Drosophila.
article_number: dev196121.
article_processing_charge: No
article_type: original
author:
- first_name: Daisy J.
  full_name: Vinter, Daisy J.
  last_name: Vinter
- first_name: Caroline
  full_name: Hoppe, Caroline
  last_name: Hoppe
- first_name: Thomas
  full_name: Minchington, Thomas
  id: 7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f
  last_name: Minchington
- first_name: Catherine
  full_name: Sutcliffe, Catherine
  last_name: Sutcliffe
- first_name: Hilary L.
  full_name: Ashe, Hilary L.
  last_name: Ashe
citation:
  ama: Vinter DJ, Hoppe C, Minchington T, Sutcliffe C, Ashe HL. Dynamics of hunchback
    translation in real-time and at single-mRNA resolution in the Drosophila embryo.
    <i>Development</i>. 2021;148(18). doi:<a href="https://doi.org/10.1242/dev.196121">10.1242/dev.196121</a>
  apa: Vinter, D. J., Hoppe, C., Minchington, T., Sutcliffe, C., &#38; Ashe, H. L.
    (2021). Dynamics of hunchback translation in real-time and at single-mRNA resolution
    in the Drosophila embryo. <i>Development</i>. The Company of Biologists. <a href="https://doi.org/10.1242/dev.196121">https://doi.org/10.1242/dev.196121</a>
  chicago: Vinter, Daisy J., Caroline Hoppe, Thomas Minchington, Catherine Sutcliffe,
    and Hilary L. Ashe. “Dynamics of Hunchback Translation in Real-Time and at Single-MRNA
    Resolution in the Drosophila Embryo.” <i>Development</i>. The Company of Biologists,
    2021. <a href="https://doi.org/10.1242/dev.196121">https://doi.org/10.1242/dev.196121</a>.
  ieee: D. J. Vinter, C. Hoppe, T. Minchington, C. Sutcliffe, and H. L. Ashe, “Dynamics
    of hunchback translation in real-time and at single-mRNA resolution in the Drosophila
    embryo,” <i>Development</i>, vol. 148, no. 18. The Company of Biologists, 2021.
  ista: Vinter DJ, Hoppe C, Minchington T, Sutcliffe C, Ashe HL. 2021. Dynamics of
    hunchback translation in real-time and at single-mRNA resolution in the Drosophila
    embryo. Development. 148(18), dev196121.
  mla: Vinter, Daisy J., et al. “Dynamics of Hunchback Translation in Real-Time and
    at Single-MRNA Resolution in the Drosophila Embryo.” <i>Development</i>, vol.
    148, no. 18, dev196121., The Company of Biologists, 2021, doi:<a href="https://doi.org/10.1242/dev.196121">10.1242/dev.196121</a>.
  short: D.J. Vinter, C. Hoppe, T. Minchington, C. Sutcliffe, H.L. Ashe, Development
    148 (2021).
date_created: 2024-04-03T07:26:41Z
date_published: 2021-09-01T00:00:00Z
date_updated: 2024-04-03T14:00:33Z
day: '01'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.196121
external_id:
  pmid:
  - '33722899 '
file:
- access_level: open_access
  checksum: 6d0533fe9c712448b3f9feb15e05ec4b
  content_type: application/pdf
  creator: dernst
  date_created: 2024-04-03T13:58:51Z
  date_updated: 2024-04-03T13:58:51Z
  file_id: '15290'
  file_name: 2021_CompanyBiologists_Vinter.pdf
  file_size: 16258500
  relation: main_file
  success: 1
file_date_updated: 2024-04-03T13:58:51Z
has_accepted_license: '1'
intvolume: '       148'
issue: '18'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
  eissn:
  - 1477-9129
  issn:
  - 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dynamics of hunchback translation in real-time and at single-mRNA resolution
  in the Drosophila embryo
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 148
year: '2021'
...
---
_id: '15272'
abstract:
- lang: eng
  text: The assembly of neuronal circuits involves the migrations of neurons from
    their place of birth to their final location in the nervous system, as well as
    the coordinated growth and patterning of axons and dendrites. In screens for genes
    required for patterning of the nervous system, we identified the <jats:italic>catp-8/P5A-ATPase</jats:italic>
    as an important regulator of neural patterning. P5A-ATPases are part of the P-type
    ATPases, a family of proteins known to serve a conserved function as transporters
    of ions, lipids and polyamines in unicellular eukaryotes, plants, and humans.
    While the function of many P-type ATPases is relatively well understood, the function
    of P5A-ATPases in metazoans remained elusive. We show here, that the <jats:italic>Caenorhabditis
    elegans</jats:italic> ortholog <jats:italic>catp-8/P5A-ATPase</jats:italic> is
    required for defined aspects of nervous system development. Specifically, the
    <jats:italic>catp-8/P5A-ATPase</jats:italic> serves functions in shaping the elaborately
    sculpted dendritic trees of somatosensory PVD neurons. Moreover, <jats:italic>catp-8/P5A-ATPase</jats:italic>
    is required for axonal guidance and repulsion at the midline, as well as embryonic
    and postembryonic neuronal migrations. Interestingly, not all axons at the midline
    require <jats:italic>catp-8/P5A-ATPase</jats:italic>, although the axons run in
    the same fascicles and navigate the same space. Similarly, not all neuronal migrations
    require <jats:italic>catp-8/P5A-ATPase</jats:italic>. A CATP-8/P5A-ATPase reporter
    is localized to the ER in most, if not all, tissues and <jats:italic>catp-8/P5A-ATPase</jats:italic>
    can function both cell-autonomously and non-autonomously to regulate neuronal
    development. Genetic analyses establish that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    can function in multiple pathways, including the Menorin pathway, previously shown
    to control dendritic patterning in PVD, and Wnt signaling, which functions to
    control neuronal migrations. Lastly, we show that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    is required for localizing select transmembrane proteins necessary for dendrite
    morphogenesis. Collectively, our studies suggest that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    serves diverse, yet specific, roles in different genetic pathways and may be involved
    in the regulation or localization of transmembrane and secreted proteins to specific
    subcellular compartments.
article_number: e1009475
article_processing_charge: No
article_type: original
author:
- first_name: Leo T. H.
  full_name: Tang, Leo T. H.
  last_name: Tang
- first_name: Meera
  full_name: Trivedi, Meera
  last_name: Trivedi
- first_name: Jenna
  full_name: Freund, Jenna
  last_name: Freund
- first_name: Christopher J.
  full_name: Salazar, Christopher J.
  last_name: Salazar
- first_name: Maisha
  full_name: Rahman, Maisha
  last_name: Rahman
- first_name: Nelson
  full_name: Ramirez, Nelson
  id: 39831956-E4FE-11E9-85DE-0DC7E5697425
  last_name: Ramirez
- first_name: Garrett
  full_name: Lee, Garrett
  last_name: Lee
- first_name: Yu
  full_name: Wang, Yu
  last_name: Wang
- first_name: Barth D.
  full_name: Grant, Barth D.
  last_name: Grant
- first_name: Hannes E.
  full_name: Bülow, Hannes E.
  last_name: Bülow
citation:
  ama: Tang LTH, Trivedi M, Freund J, et al. The CATP-8/P5A-type ATPase functions
    in multiple pathways during neuronal patterning. <i>PLOS Genetics</i>. 2021;17(7).
    doi:<a href="https://doi.org/10.1371/journal.pgen.1009475">10.1371/journal.pgen.1009475</a>
  apa: Tang, L. T. H., Trivedi, M., Freund, J., Salazar, C. J., Rahman, M., Ramirez,
    N., … Bülow, H. E. (2021). The CATP-8/P5A-type ATPase functions in multiple pathways
    during neuronal patterning. <i>PLOS Genetics</i>. Public Library of Science. <a
    href="https://doi.org/10.1371/journal.pgen.1009475">https://doi.org/10.1371/journal.pgen.1009475</a>
  chicago: Tang, Leo T. H., Meera Trivedi, Jenna Freund, Christopher J. Salazar, Maisha
    Rahman, Nelson Ramirez, Garrett Lee, Yu Wang, Barth D. Grant, and Hannes E. Bülow.
    “The CATP-8/P5A-Type ATPase Functions in Multiple Pathways during Neuronal Patterning.”
    <i>PLOS Genetics</i>. Public Library of Science, 2021. <a href="https://doi.org/10.1371/journal.pgen.1009475">https://doi.org/10.1371/journal.pgen.1009475</a>.
  ieee: L. T. H. Tang <i>et al.</i>, “The CATP-8/P5A-type ATPase functions in multiple
    pathways during neuronal patterning,” <i>PLOS Genetics</i>, vol. 17, no. 7. Public
    Library of Science, 2021.
  ista: Tang LTH, Trivedi M, Freund J, Salazar CJ, Rahman M, Ramirez N, Lee G, Wang
    Y, Grant BD, Bülow HE. 2021. The CATP-8/P5A-type ATPase functions in multiple
    pathways during neuronal patterning. PLOS Genetics. 17(7), e1009475.
  mla: Tang, Leo T. H., et al. “The CATP-8/P5A-Type ATPase Functions in Multiple Pathways
    during Neuronal Patterning.” <i>PLOS Genetics</i>, vol. 17, no. 7, e1009475, Public
    Library of Science, 2021, doi:<a href="https://doi.org/10.1371/journal.pgen.1009475">10.1371/journal.pgen.1009475</a>.
  short: L.T.H. Tang, M. Trivedi, J. Freund, C.J. Salazar, M. Rahman, N. Ramirez,
    G. Lee, Y. Wang, B.D. Grant, H.E. Bülow, PLOS Genetics 17 (2021).
date_created: 2024-04-03T07:57:12Z
date_published: 2021-07-01T00:00:00Z
date_updated: 2024-04-10T08:57:16Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1371/journal.pgen.1009475
external_id:
  pmid:
  - '34197450'
file:
- access_level: open_access
  checksum: 7352b195e4db6d404f702fe6ad8b55ad
  content_type: application/pdf
  creator: dernst
  date_created: 2024-04-10T08:53:43Z
  date_updated: 2024-04-10T08:53:43Z
  file_id: '15308'
  file_name: 2021_PlosGenetics_Tang.pdf
  file_size: 4224934
  relation: main_file
  success: 1
file_date_updated: 2024-04-10T08:53:43Z
has_accepted_license: '1'
intvolume: '        17'
issue: '7'
keyword:
- Cancer Research
- Genetics (clinical)
- Genetics
- Molecular Biology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
  issn:
  - 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: The CATP-8/P5A-type ATPase functions in multiple pathways during neuronal patterning
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2021'
...
---
_id: '15273'
abstract:
- lang: eng
  text: Synapses of glutamatergic mossy fibers (MFs) onto cerebellar unipolar brush
    cells (UBCs) generate slow excitatory (ON) or inhibitory (OFF) postsynaptic responses
    dependent on the complement of glutamate receptors expressed on the UBC’s large
    dendritic brush. Using mouse brain slice recording and computational modeling
    of synaptic transmission, we found that substantial glutamate is maintained in
    the UBC synaptic cleft, sufficient to modify spontaneous firing in OFF UBCs and
    tonically desensitize AMPARs of ON UBCs. The source of this ambient glutamate
    was spontaneous, spike-independent exocytosis from the MF terminal, and its level
    was dependent on activity of glutamate transporters EAAT1–2. Increasing levels
    of ambient glutamate shifted the polarity of evoked synaptic responses in ON UBCs
    and altered the phase of responses to in vivo-like synaptic activity. Unlike classical
    fast synapses, receptors at the UBC synapse are virtually always exposed to a
    significant level of glutamate, which varies in a graded manner during transmission.
article_number: e63819
article_processing_charge: Yes
article_type: original
author:
- first_name: Timothy S
  full_name: Balmer, Timothy S
  last_name: Balmer
- first_name: Carolina
  full_name: Borges Merjane, Carolina
  id: 4305C450-F248-11E8-B48F-1D18A9856A87
  last_name: Borges Merjane
  orcid: 0000-0003-0005-401X
- first_name: Laurence O
  full_name: Trussell, Laurence O
  last_name: Trussell
citation:
  ama: Balmer TS, Borges Merjane C, Trussell LO. Incomplete removal of extracellular
    glutamate controls synaptic transmission and integration at a cerebellar synapse.
    <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/elife.63819">10.7554/elife.63819</a>
  apa: Balmer, T. S., Borges Merjane, C., &#38; Trussell, L. O. (2021). Incomplete
    removal of extracellular glutamate controls synaptic transmission and integration
    at a cerebellar synapse. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.63819">https://doi.org/10.7554/elife.63819</a>
  chicago: Balmer, Timothy S, Carolina Borges Merjane, and Laurence O Trussell. “Incomplete
    Removal of Extracellular Glutamate Controls Synaptic Transmission and Integration
    at a Cerebellar Synapse.” <i>ELife</i>. eLife Sciences Publications, 2021. <a
    href="https://doi.org/10.7554/elife.63819">https://doi.org/10.7554/elife.63819</a>.
  ieee: T. S. Balmer, C. Borges Merjane, and L. O. Trussell, “Incomplete removal of
    extracellular glutamate controls synaptic transmission and integration at a cerebellar
    synapse,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.
  ista: Balmer TS, Borges Merjane C, Trussell LO. 2021. Incomplete removal of extracellular
    glutamate controls synaptic transmission and integration at a cerebellar synapse.
    eLife. 10, e63819.
  mla: Balmer, Timothy S., et al. “Incomplete Removal of Extracellular Glutamate Controls
    Synaptic Transmission and Integration at a Cerebellar Synapse.” <i>ELife</i>,
    vol. 10, e63819, eLife Sciences Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.63819">10.7554/elife.63819</a>.
  short: T.S. Balmer, C. Borges Merjane, L.O. Trussell, ELife 10 (2021).
date_created: 2024-04-03T07:58:11Z
date_published: 2021-02-22T00:00:00Z
date_updated: 2024-04-09T11:15:01Z
day: '22'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.7554/elife.63819
external_id:
  pmid:
  - '33616036'
file:
- access_level: open_access
  checksum: bbd4de2e54b7fbc11fba14f59e87fe3f
  content_type: application/pdf
  creator: dernst
  date_created: 2024-04-09T11:13:07Z
  date_updated: 2024-04-09T11:13:07Z
  file_id: '15307'
  file_name: 2021_eLife_Balmer.pdf
  file_size: 6997954
  relation: main_file
  success: 1
file_date_updated: 2024-04-09T11:13:07Z
has_accepted_license: '1'
intvolume: '        10'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Incomplete removal of extracellular glutamate controls synaptic transmission
  and integration at a cerebellar synapse
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2021'
...
---
_id: '15276'
abstract:
- lang: eng
  text: Biotrophic plant pathogens secrete effector proteins to manipulate the host
    physiology. Effectors suppress defenses and induce an environment favorable to
    disease development. Sequence-based prediction of effector function is impeded
    by their rapid evolution rate. In the maize pathogen <jats:italic>Ustilago maydis</jats:italic>,
    effector-coding genes frequently organize in clusters. Here we describe the functional
    characterization of the <jats:italic>pleiades</jats:italic>, a cluster of ten
    effector genes, by analyzing the micro- and macroscopic phenotype of the cluster
    deletion and expressing these proteins <jats:italic>in planta</jats:italic>. Deletion
    of the <jats:italic>pleiades</jats:italic> leads to strongly impaired virulence
    and accumulation of reactive oxygen species (ROS) in infected tissue. Eight of
    the Pleiades suppress the production of ROS upon perception of pathogen associated
    molecular patterns (PAMPs). Although functionally redundant, the Pleiades target
    different host components. The paralogs Taygeta1 and Merope1 suppress ROS production
    in either the cytoplasm or nucleus, respectively. Merope1 targets and promotes
    the auto-ubiquitination activity of RFI2, a conserved family of E3 ligases that
    regulates the production of PAMP-triggered ROS burst in plants.
article_number: e1009641
article_processing_charge: Yes
article_type: original
author:
- first_name: Fernando
  full_name: Navarrete, Fernando
  last_name: Navarrete
- first_name: Nenad
  full_name: Grujic, Nenad
  last_name: Grujic
- first_name: Alexandra
  full_name: Stirnberg, Alexandra
  last_name: Stirnberg
- first_name: Indira
  full_name: Saado, Indira
  last_name: Saado
- first_name: David
  full_name: Aleksza, David
  last_name: Aleksza
- first_name: Michelle C
  full_name: Gallei, Michelle C
  id: 35A03822-F248-11E8-B48F-1D18A9856A87
  last_name: Gallei
  orcid: 0000-0003-1286-7368
- first_name: Hazem
  full_name: Adi, Hazem
  last_name: Adi
- first_name: André
  full_name: Alcântara, André
  last_name: Alcântara
- first_name: Mamoona
  full_name: Khan, Mamoona
  last_name: Khan
- first_name: Janos
  full_name: Bindics, Janos
  last_name: Bindics
- first_name: Marco
  full_name: Trujillo, Marco
  last_name: Trujillo
- first_name: Armin
  full_name: Djamei, Armin
  last_name: Djamei
citation:
  ama: Navarrete F, Grujic N, Stirnberg A, et al. The Pleiades are a cluster of fungal
    effectors that inhibit host defenses. <i>PLOS Pathogens</i>. 2021;17(6). doi:<a
    href="https://doi.org/10.1371/journal.ppat.1009641">10.1371/journal.ppat.1009641</a>
  apa: Navarrete, F., Grujic, N., Stirnberg, A., Saado, I., Aleksza, D., Gallei, M.
    C., … Djamei, A. (2021). The Pleiades are a cluster of fungal effectors that inhibit
    host defenses. <i>PLOS Pathogens</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.ppat.1009641">https://doi.org/10.1371/journal.ppat.1009641</a>
  chicago: Navarrete, Fernando, Nenad Grujic, Alexandra Stirnberg, Indira Saado, David
    Aleksza, Michelle C Gallei, Hazem Adi, et al. “The Pleiades Are a Cluster of Fungal
    Effectors That Inhibit Host Defenses.” <i>PLOS Pathogens</i>. Public Library of
    Science, 2021. <a href="https://doi.org/10.1371/journal.ppat.1009641">https://doi.org/10.1371/journal.ppat.1009641</a>.
  ieee: F. Navarrete <i>et al.</i>, “The Pleiades are a cluster of fungal effectors
    that inhibit host defenses,” <i>PLOS Pathogens</i>, vol. 17, no. 6. Public Library
    of Science, 2021.
  ista: Navarrete F, Grujic N, Stirnberg A, Saado I, Aleksza D, Gallei MC, Adi H,
    Alcântara A, Khan M, Bindics J, Trujillo M, Djamei A. 2021. The Pleiades are a
    cluster of fungal effectors that inhibit host defenses. PLOS Pathogens. 17(6),
    e1009641.
  mla: Navarrete, Fernando, et al. “The Pleiades Are a Cluster of Fungal Effectors
    That Inhibit Host Defenses.” <i>PLOS Pathogens</i>, vol. 17, no. 6, e1009641,
    Public Library of Science, 2021, doi:<a href="https://doi.org/10.1371/journal.ppat.1009641">10.1371/journal.ppat.1009641</a>.
  short: F. Navarrete, N. Grujic, A. Stirnberg, I. Saado, D. Aleksza, M.C. Gallei,
    H. Adi, A. Alcântara, M. Khan, J. Bindics, M. Trujillo, A. Djamei, PLOS Pathogens
    17 (2021).
date_created: 2024-04-03T08:00:34Z
date_published: 2021-06-24T00:00:00Z
date_updated: 2024-04-09T10:26:12Z
day: '24'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1371/journal.ppat.1009641
external_id:
  pmid:
  - '34166468'
file:
- access_level: open_access
  checksum: ab8428291a0c14607c4ea5656c029cff
  content_type: application/pdf
  creator: dernst
  date_created: 2024-04-09T10:24:43Z
  date_updated: 2024-04-09T10:24:43Z
  file_id: '15305'
  file_name: 2021_PlosPathogens_Navarrete.pdf
  file_size: 2616563
  relation: main_file
  success: 1
file_date_updated: 2024-04-09T10:24:43Z
has_accepted_license: '1'
intvolume: '        17'
issue: '6'
keyword:
- Virology
- Genetics
- Molecular Biology
- Immunology
- Microbiology
- Parasitology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Pathogens
publication_identifier:
  issn:
  - 1553-7374
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: The Pleiades are a cluster of fungal effectors that inhibit host defenses
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2021'
...
---
_id: '10834'
abstract:
- lang: eng
  text: Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE
    regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation
    and the protrusion of branched actin filament networks. Moreover, Hem1 loss of
    function in immune cells causes autoimmune diseases in humans. Here, we show that
    genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis
    as well as phagocytic cup formation in addition to defects in lamellipodial protrusion
    and migration. Moreover, Hem1-null macrophages displayed strong defects in cell
    adhesion despite unaltered podosome formation and concomitant extracellular matrix
    degradation. Specifically, dynamics of both adhesion and de-adhesion as well as
    concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly
    compromised. Accordingly, disruption of WRC function in non-hematopoietic cells
    coincided with both defects in adhesion turnover and altered FAK and paxillin
    phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished
    integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes,
    but not lamellipodia formation, were partially rescued by small molecule activation
    of FAK. A full rescue of the phenotype, including lamellipodia formation, required
    not only the presence of WRCs but also their binding to and activation by Rac.
    Collectively, our results uncover that WRC impacts on integrin-dependent processes
    in a FAK-dependent manner, controlling formation and dismantling of adhesions,
    relevant for properly grabbing onto extracellular surfaces and particles during
    cell edge expansion, like in migration or phagocytosis.
acknowledgement: We are grateful to Silvia Prettin, Ina Schleicher, and Petra Hagendorff
  for expert technical assistance; David Dettbarn for animal keeping and breeding;
  and Lothar Gröbe and Maria Höxter for cell sorting. We also thank Werner Tegge for
  peptides and Giorgio Scita for antibodies. This work was supported, in part, by
  the Deutsche Forschungsgemeinschaft (DFG), Priority Programm SPP1150 (to T.E.B.S.,
  K.R., and M. Sixt), and by DFG grant GRK2223/1 (to K.R.). T.E.B.S. acknowledges
  support by the Helmholtz Society through HGF impulse fund W2/W3-066 and M. Schnoor
  by the Mexican Council for Science and Technology (CONACyT, 284292 ), Fund SEP-Cinvestav
  ( 108 ), and the Royal Society, UK (Newton Advanced Fellowship, NAF/R1/180017 ).
article_processing_charge: No
article_type: original
author:
- first_name: Stephanie
  full_name: Stahnke, Stephanie
  last_name: Stahnke
- first_name: Hermann
  full_name: Döring, Hermann
  last_name: Döring
- first_name: Charly
  full_name: Kusch, Charly
  last_name: Kusch
- first_name: David J.J.
  full_name: de Gorter, David J.J.
  last_name: de Gorter
- first_name: Sebastian
  full_name: Dütting, Sebastian
  last_name: Dütting
- first_name: Aleks
  full_name: Guledani, Aleks
  last_name: Guledani
- first_name: Irina
  full_name: Pleines, Irina
  last_name: Pleines
- first_name: Michael
  full_name: Schnoor, Michael
  last_name: Schnoor
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Robert
  full_name: Geffers, Robert
  last_name: Geffers
- first_name: Manfred
  full_name: Rohde, Manfred
  last_name: Rohde
- first_name: Mathias
  full_name: Müsken, Mathias
  last_name: Müsken
- first_name: Frieda
  full_name: Kage, Frieda
  last_name: Kage
- first_name: Anika
  full_name: Steffen, Anika
  last_name: Steffen
- first_name: Jan
  full_name: Faix, Jan
  last_name: Faix
- first_name: Bernhard
  full_name: Nieswandt, Bernhard
  last_name: Nieswandt
- first_name: Klemens
  full_name: Rottner, Klemens
  last_name: Rottner
- first_name: Theresia E.B.
  full_name: Stradal, Theresia E.B.
  last_name: Stradal
citation:
  ama: Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function
    and impacts migration, phagocytosis, and integrin-mediated adhesion. <i>Current
    Biology</i>. 2021;31(10):2051-2064.e8. doi:<a href="https://doi.org/10.1016/j.cub.2021.02.043">10.1016/j.cub.2021.02.043</a>
  apa: Stahnke, S., Döring, H., Kusch, C., de Gorter, D. J. J., Dütting, S., Guledani,
    A., … Stradal, T. E. B. (2021). Loss of Hem1 disrupts macrophage function and
    impacts migration, phagocytosis, and integrin-mediated adhesion. <i>Current Biology</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.cub.2021.02.043">https://doi.org/10.1016/j.cub.2021.02.043</a>
  chicago: Stahnke, Stephanie, Hermann Döring, Charly Kusch, David J.J. de Gorter,
    Sebastian Dütting, Aleks Guledani, Irina Pleines, et al. “Loss of Hem1 Disrupts
    Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated
    Adhesion.” <i>Current Biology</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.cub.2021.02.043">https://doi.org/10.1016/j.cub.2021.02.043</a>.
  ieee: S. Stahnke <i>et al.</i>, “Loss of Hem1 disrupts macrophage function and impacts
    migration, phagocytosis, and integrin-mediated adhesion,” <i>Current Biology</i>,
    vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021.
  ista: Stahnke S, Döring H, Kusch C, de Gorter DJJ, Dütting S, Guledani A, Pleines
    I, Schnoor M, Sixt MK, Geffers R, Rohde M, Müsken M, Kage F, Steffen A, Faix J,
    Nieswandt B, Rottner K, Stradal TEB. 2021. Loss of Hem1 disrupts macrophage function
    and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology.
    31(10), 2051–2064.e8.
  mla: Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts
    Migration, Phagocytosis, and Integrin-Mediated Adhesion.” <i>Current Biology</i>,
    vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:<a href="https://doi.org/10.1016/j.cub.2021.02.043">10.1016/j.cub.2021.02.043</a>.
  short: S. Stahnke, H. Döring, C. Kusch, D.J.J. de Gorter, S. Dütting, A. Guledani,
    I. Pleines, M. Schnoor, M.K. Sixt, R. Geffers, M. Rohde, M. Müsken, F. Kage, A.
    Steffen, J. Faix, B. Nieswandt, K. Rottner, T.E.B. Stradal, Current Biology 31
    (2021) 2051–2064.e8.
date_created: 2022-03-08T07:51:04Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2023-08-17T07:01:14Z
day: '24'
department:
- _id: MiSi
doi: 10.1016/j.cub.2021.02.043
external_id:
  isi:
  - '000654652200002'
  pmid:
  - '33711252'
intvolume: '        31'
isi: 1
issue: '10'
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/2020.03.24.005835
month: '05'
oa: 1
oa_version: Preprint
page: 2051-2064.e8
pmid: 1
publication: Current Biology
publication_identifier:
  issn:
  - 0960-9822
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis,
  and integrin-mediated adhesion
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 31
year: '2021'
...
---
_id: '11052'
abstract:
- lang: eng
  text: In order to combat molecular damage, most cellular proteins undergo rapid
    turnover. We have previously identified large nuclear protein assemblies that
    can persist for years in post-mitotic tissues and are subject to age-related decline.
    Here, we report that mitochondria can be long lived in the mouse brain and reveal
    that specific mitochondrial proteins have half-lives longer than the average proteome.
    These mitochondrial long-lived proteins (mitoLLPs) are core components of the
    electron transport chain (ETC) and display increased longevity in respiratory
    supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site
    between complexes I and IV, is required for complex IV and supercomplex assembly.
    Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained
    for days, effectively uncoupling mitochondrial function from ongoing transcription
    of its mitoLLPs. Our results suggest that modulating protein longevity within
    the ETC is critical for mitochondrial proteome maintenance and the robustness
    of mitochondrial function.
article_processing_charge: No
article_type: original
author:
- first_name: Shefali
  full_name: Krishna, Shefali
  last_name: Krishna
- first_name: Rafael
  full_name: Arrojo e Drigo, Rafael
  last_name: Arrojo e Drigo
- first_name: Juliana S.
  full_name: Capitanio, Juliana S.
  last_name: Capitanio
- first_name: Ranjan
  full_name: Ramachandra, Ranjan
  last_name: Ramachandra
- first_name: Mark
  full_name: Ellisman, Mark
  last_name: Ellisman
- first_name: Martin W
  full_name: HETZER, Martin W
  id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
  last_name: HETZER
  orcid: 0000-0002-2111-992X
citation:
  ama: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
    M. Identification of long-lived proteins in the mitochondria reveals increased
    stability of the electron transport chain. <i>Developmental Cell</i>. 2021;56(21):P2952-2965.e9.
    doi:<a href="https://doi.org/10.1016/j.devcel.2021.10.008">10.1016/j.devcel.2021.10.008</a>
  apa: Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman,
    M., &#38; Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria
    reveals increased stability of the electron transport chain. <i>Developmental
    Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.devcel.2021.10.008">https://doi.org/10.1016/j.devcel.2021.10.008</a>
  chicago: Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra,
    Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the
    Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental
    Cell</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.devcel.2021.10.008">https://doi.org/10.1016/j.devcel.2021.10.008</a>.
  ieee: S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman,
    and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals
    increased stability of the electron transport chain,” <i>Developmental Cell</i>,
    vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.
  ista: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
    M. 2021. Identification of long-lived proteins in the mitochondria reveals increased
    stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.
  mla: Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria
    Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental
    Cell</i>, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:<a href="https://doi.org/10.1016/j.devcel.2021.10.008">10.1016/j.devcel.2021.10.008</a>.
  short: S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman,
    M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.
date_created: 2022-04-07T07:43:14Z
date_published: 2021-11-08T00:00:00Z
date_updated: 2025-12-15T10:01:56Z
day: '08'
department:
- _id: MaHe
doi: 10.1016/j.devcel.2021.10.008
extern: '1'
external_id:
  pmid:
  - '34715012'
intvolume: '        56'
issue: '21'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa_version: None
page: P2952-2965.e9
pmid: 1
publication: Developmental Cell
publication_identifier:
  issn:
  - 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of long-lived proteins in the mitochondria reveals increased
  stability of the electron transport chain
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2021'
...
---
_id: '10163'
abstract:
- lang: eng
  text: The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol
    II) is a regulatory hub for transcription and RNA processing. Here, we identify
    PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability
    that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a
    CTD reader domain that preferentially binds two phosphorylated Serine-2 marks
    in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated
    Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length
    of genes. PHF3 knock-out or SPOC deletion in human cells results in increased
    Pol II stalling, reduced elongation rate and an increase in mRNA stability, with
    marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed
    in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation.
    Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation
    by bridging transcription with mRNA decay.
acknowledgement: 'D.S. thanks Claudine Kraft, Renée Schroeder, Verena Jantsch, Franz
  Klein and Peter Schlögelhofer for support. We thank Anita Testa Salmazo for help
  with purifying Pol II; Matthias Geyer and Robert Düster for sharing DYRK1A kinase;
  Felix Hartmann and Clemens Plaschka for help with mass photometry; Goran Kokic for
  design of the arrest assay sequences; Petra van der Lelij for help with generating
  mESC KO; Maximilian Freilinger for help with the purification of mEGFP-CTD; Stefan
  Ameres, Nina Fasching and Brian Reichholf for advice on SLAM-seq and for sharing
  reagents; Laura Gallego Valle for advice regarding LLPS assays; Krzysztof Chylinski
  for advice regarding CRISPR/Cas9 methodology; VBCF Protein Technologies facility
  for purifying PHF3 and providing gRNAs and Cas9; VBCF NGS facility for sequencing;
  Monoclonal antibody facility at the Helmholtz center for Pol II antibodies; Friedrich
  Propst and Elzbieta Kowalska for advice and for sharing materials; Egon Ogris for
  sharing materials; Martin Eilers for recommending a ChIP-grade TFIIS antibody; Susanne
  Opravil, Otto Hudecz, Markus Hartl and Natascha Hartl for mass spectrometry analysis;
  staff of the X-ray beamlines at the ESRF in Grenoble for their excellent support;
  Christa Bücker, Anton Meinhart, Clemens Plaschka and members of the Slade lab for
  critical comments on the manuscript; Life Science Editors for editing assistance.
  M.B. and D.S. acknowledge support by the FWF-funded DK ‘Chromosome Dynamics’. T.K.
  is a recipient of the DOC fellowship from the Austrian Academy of Sciences. U.S.
  is supported by the L’Oreal for Women in Science Austria Fellowship and the Austrian
  Science Fund (FWF T 795-B30). M.L is supported by the Vienna Science and Technology
  Fund (WWTF, VRG14-006). R.S. is supported by the Czech Science Foundation (15-17670 S
  and 21-24460 S), Ministry of Education, Youths and Sports of the Czech Republic
  (CEITEC 2020 project (LQ1601)), and the European Research Council (ERC) under the
  European Union’s Horizon 2020 research and innovation programme (Grant agreement
  no. 649030); this publication reflects only the author’s view and the Research Executive
  Agency is not responsible for any use that may be made of the information it contains.
  M.S. is supported by the Czech Science Foundation (GJ20-21581Y). K.D.C. research
  is supported by the Austrian Science Fund (FWF) Projects I525 and I1593, P22276,
  P19060, and W1221, Federal Ministry of Economy, Family and Youth through the initiative
  ‘Laura Bassi Centres of Expertise’, funding from the Centre of Optimized Structural
  Studies No. 253275, the Wellcome Trust Collaborative Award (201543/Z/16), COST action
  BM1405 Non-globular proteins - from sequence to structure, function and application
  in molecular physiopathology (NGP-NET), the Vienna Science and Technology Fund (WWTF
  LS17-008), and by the University of Vienna. This project was funded by the MFPL
  start-up grant, the Vienna Science and Technology Fund (WWTF LS14-001), and the
  Austrian Science Fund (P31546-B28 and W1258 “DK: Integrative Structural Biology”)
  to D.S.'
article_number: '6078'
article_processing_charge: No
article_type: original
author:
- first_name: Lisa-Marie
  full_name: Appel, Lisa-Marie
  last_name: Appel
- first_name: Vedran
  full_name: Franke, Vedran
  last_name: Franke
- first_name: Melania
  full_name: Bruno, Melania
  last_name: Bruno
- first_name: Irina
  full_name: Grishkovskaya, Irina
  last_name: Grishkovskaya
- first_name: Aiste
  full_name: Kasiliauskaite, Aiste
  last_name: Kasiliauskaite
- first_name: Tanja
  full_name: Kaufmann, Tanja
  last_name: Kaufmann
- first_name: Ursula E.
  full_name: Schoeberl, Ursula E.
  last_name: Schoeberl
- first_name: Martin G.
  full_name: Puchinger, Martin G.
  last_name: Puchinger
- first_name: Sebastian
  full_name: Kostrhon, Sebastian
  last_name: Kostrhon
- first_name: Carmen
  full_name: Ebenwaldner, Carmen
  last_name: Ebenwaldner
- first_name: Marek
  full_name: Sebesta, Marek
  last_name: Sebesta
- first_name: Etienne
  full_name: Beltzung, Etienne
  last_name: Beltzung
- first_name: Karl
  full_name: Mechtler, Karl
  last_name: Mechtler
- first_name: Gen
  full_name: Lin, Gen
  last_name: Lin
- first_name: Anna
  full_name: Vlasova, Anna
  last_name: Vlasova
- first_name: Martin
  full_name: Leeb, Martin
  last_name: Leeb
- first_name: Rushad
  full_name: Pavri, Rushad
  last_name: Pavri
- first_name: Alexander
  full_name: Stark, Alexander
  last_name: Stark
- first_name: Altuna
  full_name: Akalin, Altuna
  last_name: Akalin
- first_name: Richard
  full_name: Stefl, Richard
  last_name: Stefl
- first_name: Carrie A
  full_name: Bernecky, Carrie A
  id: 2CB9DFE2-F248-11E8-B48F-1D18A9856A87
  last_name: Bernecky
  orcid: 0000-0003-0893-7036
- first_name: Kristina
  full_name: Djinovic-Carugo, Kristina
  last_name: Djinovic-Carugo
- first_name: Dea
  full_name: Slade, Dea
  last_name: Slade
citation:
  ama: Appel L-M, Franke V, Bruno M, et al. PHF3 regulates neuronal gene expression
    through the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. 2021;12(1).
    doi:<a href="https://doi.org/10.1038/s41467-021-26360-2">10.1038/s41467-021-26360-2</a>
  apa: Appel, L.-M., Franke, V., Bruno, M., Grishkovskaya, I., Kasiliauskaite, A.,
    Kaufmann, T., … Slade, D. (2021). PHF3 regulates neuronal gene expression through
    the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. Springer Nature.
    <a href="https://doi.org/10.1038/s41467-021-26360-2">https://doi.org/10.1038/s41467-021-26360-2</a>
  chicago: Appel, Lisa-Marie, Vedran Franke, Melania Bruno, Irina Grishkovskaya, Aiste
    Kasiliauskaite, Tanja Kaufmann, Ursula E. Schoeberl, et al. “PHF3 Regulates Neuronal
    Gene Expression through the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>.
    Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-26360-2">https://doi.org/10.1038/s41467-021-26360-2</a>.
  ieee: L.-M. Appel <i>et al.</i>, “PHF3 regulates neuronal gene expression through
    the Pol II CTD reader domain SPOC,” <i>Nature Communications</i>, vol. 12, no.
    1. Springer Nature, 2021.
  ista: Appel L-M, Franke V, Bruno M, Grishkovskaya I, Kasiliauskaite A, Kaufmann
    T, Schoeberl UE, Puchinger MG, Kostrhon S, Ebenwaldner C, Sebesta M, Beltzung
    E, Mechtler K, Lin G, Vlasova A, Leeb M, Pavri R, Stark A, Akalin A, Stefl R,
    Bernecky C, Djinovic-Carugo K, Slade D. 2021. PHF3 regulates neuronal gene expression
    through the Pol II CTD reader domain SPOC. Nature Communications. 12(1), 6078.
  mla: Appel, Lisa-Marie, et al. “PHF3 Regulates Neuronal Gene Expression through
    the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>, vol. 12, no.
    1, 6078, Springer Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-26360-2">10.1038/s41467-021-26360-2</a>.
  short: L.-M. Appel, V. Franke, M. Bruno, I. Grishkovskaya, A. Kasiliauskaite, T.
    Kaufmann, U.E. Schoeberl, M.G. Puchinger, S. Kostrhon, C. Ebenwaldner, M. Sebesta,
    E. Beltzung, K. Mechtler, G. Lin, A. Vlasova, M. Leeb, R. Pavri, A. Stark, A.
    Akalin, R. Stefl, C. Bernecky, K. Djinovic-Carugo, D. Slade, Nature Communications
    12 (2021).
date_created: 2021-10-20T14:40:32Z
date_published: 2021-10-19T00:00:00Z
date_updated: 2024-10-21T06:02:05Z
day: '19'
ddc:
- '610'
department:
- _id: CaBe
doi: 10.1038/s41467-021-26360-2
external_id:
  isi:
  - '000709050300001'
file:
- access_level: open_access
  checksum: d99fcd51aebde19c21314e3de0148007
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-10-21T13:51:49Z
  date_updated: 2021-10-21T13:51:49Z
  file_id: '10169'
  file_name: 2021_NatComm_Appel.pdf
  file_size: 5111706
  relation: main_file
  success: 1
file_date_updated: 2021-10-21T13:51:49Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  link:
  - description: 'Preprint '
    relation: earlier_version
    url: https://www.biorxiv.org/content/10.1101/2020.02.11.943159
scopus_import: '1'
status: public
title: PHF3 regulates neuronal gene expression through the Pol II CTD reader domain
  SPOC
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10301'
abstract:
- lang: eng
  text: De novo protein synthesis is required for synapse modifications underlying
    stable memory encoding. Yet neurons are highly compartmentalized cells and how
    protein synthesis can be regulated at the synapse level is unknown. Here, we characterize
    neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic
    target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to
    mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A
    subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR
    complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR
    activation and restricts the mTOR-dependent translation of specific activity-regulated
    mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent
    protein synthesis, and facilitates the consolidation of associative and spatial
    memories in mice. The memory enhancement becomes evident with light or spaced
    training, can be achieved by selectively deleting GluN3A from excitatory neurons
    during adulthood, and does not compromise other aspects of cognition such as memory
    flexibility or extinction. Our findings provide mechanistic insight into synaptic
    translational control and reveal a potentially selective target for cognitive
    enhancement.
acknowledgement: We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a
  knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral
  and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and
  Ana Navarro for expert technical help. Work was funded by the UTE project CIMA;
  fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO
  (to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.),
  FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.);
  ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program
  RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077
  FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637)
  and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator
  Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R),
  Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence
  Awards (SEV-2013-0317, SEV-2017-0723).
article_number: e71575
article_processing_charge: No
article_type: original
author:
- first_name: María J
  full_name: Conde-Dusman, María J
  last_name: Conde-Dusman
- first_name: Partha N
  full_name: Dey, Partha N
  last_name: Dey
- first_name: Óscar
  full_name: Elía-Zudaire, Óscar
  last_name: Elía-Zudaire
- first_name: Luis E
  full_name: Garcia Rabaneda, Luis E
  id: 33D1B084-F248-11E8-B48F-1D18A9856A87
  last_name: Garcia Rabaneda
- first_name: Carmen
  full_name: García-Lira, Carmen
  last_name: García-Lira
- first_name: Teddy
  full_name: Grand, Teddy
  last_name: Grand
- first_name: Victor
  full_name: Briz, Victor
  last_name: Briz
- first_name: Eric R
  full_name: Velasco, Eric R
  last_name: Velasco
- first_name: Raül
  full_name: Andero Galí, Raül
  last_name: Andero Galí
- first_name: Sergio
  full_name: Niñerola, Sergio
  last_name: Niñerola
- first_name: Angel
  full_name: Barco, Angel
  last_name: Barco
- first_name: Pierre
  full_name: Paoletti, Pierre
  last_name: Paoletti
- first_name: John F
  full_name: Wesseling, John F
  last_name: Wesseling
- first_name: Fabrizio
  full_name: Gardoni, Fabrizio
  last_name: Gardoni
- first_name: Steven J
  full_name: Tavalin, Steven J
  last_name: Tavalin
- first_name: Isabel
  full_name: Perez-Otaño, Isabel
  last_name: Perez-Otaño
citation:
  ama: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis
    and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
    <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/elife.71575">10.7554/elife.71575</a>
  apa: Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E.,
    García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis
    and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
    <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.71575">https://doi.org/10.7554/elife.71575</a>
  chicago: Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia
    Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein
    Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1
    Assembly.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/elife.71575">https://doi.org/10.7554/elife.71575</a>.
  ieee: M. J. Conde-Dusman <i>et al.</i>, “Control of protein synthesis and memory
    by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” <i>eLife</i>,
    vol. 10. eLife Sciences Publications, 2021.
  ista: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C,
    Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling
    JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and
    memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife.
    10, e71575.
  mla: Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by
    GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>,
    vol. 10, e71575, eLife Sciences Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.71575">10.7554/elife.71575</a>.
  short: M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira,
    T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti,
    J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).
date_created: 2021-11-18T06:59:45Z
date_published: 2021-11-17T00:00:00Z
date_updated: 2024-10-21T06:02:05Z
day: '17'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.7554/elife.71575
external_id:
  isi:
  - '000720945900001'
file:
- access_level: open_access
  checksum: 59318e9e41507cec83c2f4070e6ad540
  content_type: application/pdf
  creator: lgarciar
  date_created: 2021-11-18T07:02:02Z
  date_updated: 2021-11-18T07:02:02Z
  file_id: '10302'
  file_name: elife-71575-v1.pdf
  file_size: 2477302
  relation: main_file
  success: 1
file_date_updated: 2021-11-18T07:02:02Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition
  of GIT1/mTORC1 assembly
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '10310'
abstract:
- lang: eng
  text: A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI)
    from Thermosynechococcus elongatus was reported as the first atomic model of PSI
    almost 20 years ago. However, the monomeric PSI structure has not yet been reported
    despite long-standing interest in its structure and extensive spectroscopic characterization
    of the loss of red chlorophylls upon monomerization. Here, we describe the structure
    of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the
    trimer structure gave detailed insights into monomerization-induced changes in
    both the central trimerization domain and the peripheral regions of the complex.
    Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls
    adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization
    of red chlorophylls and that lipids of the surrounding membrane present a major
    source of thermal energy for uphill excitation energy transfer from red chlorophylls
    to P700.
acknowledgement: We are grateful for additional support and valuable scientific input
  for this project by Yuko Misumi, Jiannan Li, Hisako Kubota-Kawai, Takeshi Kawabata,
  Mian Wu, Eiki Yamashita, Atsushi Nakagawa, Volker Hartmann, Melanie Völkel and Matthias
  Rögner. Parts of this research were funded by the German Research Council (DFG)
  within the framework of GRK 2341 (Microbial Substrate Conversion) to M.M.N., the
  Platform Project for Supporting Drug Discovery and Life Science Research [Basis
  for Supporting Innovative Drug Discovery and Life Science Research (BINDS)] from
  AMED under grant number JP20am0101117 (K.N.), JP16K07266 to Atsunori Oshima and
  C.G., a Grants-in-Aid for Scientific Research under grant number JP 25000013 (K.N.),
  17H03647 (C.G.) and 16H06560 (G.K.) from MEXT-KAKENHI, the International Joint Research
  Promotion Program from Osaka University to M.M.N., C.G. and G.K., and the Cyclic
  Innovation for Clinical Empowerment (CiCLE) Grant Number JP17pc0101020 from AMED
  to K.N. and G.K.
article_number: '304'
article_processing_charge: No
article_type: original
author:
- first_name: Mehmet Orkun
  full_name: Çoruh, Mehmet Orkun
  id: d25163e5-8d53-11eb-a251-e6dd8ea1b8ef
  last_name: Çoruh
  orcid: 0000-0002-3219-2022
- first_name: Anna
  full_name: Frank, Anna
  last_name: Frank
- first_name: Hideaki
  full_name: Tanaka, Hideaki
  last_name: Tanaka
- first_name: Akihiro
  full_name: Kawamoto, Akihiro
  last_name: Kawamoto
- first_name: Eithar
  full_name: El-Mohsnawy, Eithar
  last_name: El-Mohsnawy
- first_name: Takayuki
  full_name: Kato, Takayuki
  last_name: Kato
- first_name: Keiichi
  full_name: Namba, Keiichi
  last_name: Namba
- first_name: Christoph
  full_name: Gerle, Christoph
  last_name: Gerle
- first_name: Marc M.
  full_name: Nowaczyk, Marc M.
  last_name: Nowaczyk
- first_name: Genji
  full_name: Kurisu, Genji
  last_name: Kurisu
citation:
  ama: Çoruh MO, Frank A, Tanaka H, et al. Cryo-EM structure of a functional monomeric
    Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster.
    <i>Communications Biology</i>. 2021;4(1). doi:<a href="https://doi.org/10.1038/s42003-021-01808-9">10.1038/s42003-021-01808-9</a>
  apa: Çoruh, M. O., Frank, A., Tanaka, H., Kawamoto, A., El-Mohsnawy, E., Kato, T.,
    … Kurisu, G. (2021). Cryo-EM structure of a functional monomeric Photosystem I
    from Thermosynechococcus elongatus reveals red chlorophyll cluster. <i>Communications
    Biology</i>. Springer . <a href="https://doi.org/10.1038/s42003-021-01808-9">https://doi.org/10.1038/s42003-021-01808-9</a>
  chicago: Çoruh, Mehmet Orkun, Anna Frank, Hideaki Tanaka, Akihiro Kawamoto, Eithar
    El-Mohsnawy, Takayuki Kato, Keiichi Namba, Christoph Gerle, Marc M. Nowaczyk,
    and Genji Kurisu. “Cryo-EM Structure of a Functional Monomeric Photosystem I from
    Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications
    Biology</i>. Springer , 2021. <a href="https://doi.org/10.1038/s42003-021-01808-9">https://doi.org/10.1038/s42003-021-01808-9</a>.
  ieee: M. O. Çoruh <i>et al.</i>, “Cryo-EM structure of a functional monomeric Photosystem
    I from Thermosynechococcus elongatus reveals red chlorophyll cluster,” <i>Communications
    Biology</i>, vol. 4, no. 1. Springer , 2021.
  ista: Çoruh MO, Frank A, Tanaka H, Kawamoto A, El-Mohsnawy E, Kato T, Namba K, Gerle
    C, Nowaczyk MM, Kurisu G. 2021. Cryo-EM structure of a functional monomeric Photosystem
    I from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
    Biology. 4(1), 304.
  mla: Çoruh, Mehmet Orkun, et al. “Cryo-EM Structure of a Functional Monomeric Photosystem
    I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications
    Biology</i>, vol. 4, no. 1, 304, Springer , 2021, doi:<a href="https://doi.org/10.1038/s42003-021-01808-9">10.1038/s42003-021-01808-9</a>.
  short: M.O. Çoruh, A. Frank, H. Tanaka, A. Kawamoto, E. El-Mohsnawy, T. Kato, K.
    Namba, C. Gerle, M.M. Nowaczyk, G. Kurisu, Communications Biology 4 (2021).
date_created: 2021-11-19T11:37:29Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2023-08-14T11:51:19Z
day: '08'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.1038/s42003-021-01808-9
external_id:
  isi:
  - '000627440700001'
  pmid:
  - '33686186'
file:
- access_level: open_access
  checksum: 8ffd39f2bba7152a2441802ff313bf0b
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-11-19T15:09:18Z
  date_updated: 2021-11-19T15:09:18Z
  file_id: '10318'
  file_name: 2021_CommBio_Çoruh.pdf
  file_size: 6030261
  relation: main_file
  success: 1
file_date_updated: 2021-11-19T15:09:18Z
has_accepted_license: '1'
intvolume: '         4'
isi: 1
issue: '1'
keyword:
- general agricultural and biological Sciences
- general biochemistry
- genetics and molecular biology
- medicine (miscellaneous)
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: Communications Biology
publication_identifier:
  issn:
  - 2399-3642
publication_status: published
publisher: 'Springer '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus
  elongatus reveals red chlorophyll cluster
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2021'
...
---
_id: '10533'
abstract:
- lang: eng
  text: Flowering plants utilize small RNA molecules to guide DNA methyltransferases
    to genomic sequences. This RNA-directed DNA methylation (RdDM) pathway preferentially
    targets euchromatic transposable elements. However, RdDM is thought to be recruited
    by methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin.
    How RdDM is targeted to euchromatin despite an affinity for H3K9me is unclear.
    Here we show that loss of histone H1 enhances heterochromatic RdDM, preferentially
    at nucleosome linker DNA. Surprisingly, this does not require SHH1, the RdDM component
    that binds H3K9me. Furthermore, H3K9me is dispensable for RdDM, as is CG DNA methylation.
    Instead, we find that non-CG methylation is specifically associated with small
    RNA biogenesis, and without H1 small RNA production quantitatively expands to
    non-CG methylated loci. Our results demonstrate that H1 enforces the separation
    of euchromatic and heterochromatic DNA methylation pathways by excluding the small
    RNA-generating branch of RdDM from non-CG methylated heterochromatin.
acknowledgement: We thank X Feng for helpful comments on the manuscript. This work
  was supported by a European Research Council grant MaintainMeth (725746) to DZ.
article_number: e72676
article_processing_charge: No
article_type: original
author:
- first_name: Jaemyung
  full_name: Choi, Jaemyung
  last_name: Choi
- first_name: David B
  full_name: Lyons, David B
  last_name: Lyons
- first_name: Daniel
  full_name: Zilberman, Daniel
  id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
  last_name: Zilberman
  orcid: 0000-0002-0123-8649
citation:
  ama: Choi J, Lyons DB, Zilberman D. Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin. <i>eLife</i>. 2021;10. doi:<a
    href="https://doi.org/10.7554/elife.72676">10.7554/elife.72676</a>
  apa: Choi, J., Lyons, D. B., &#38; Zilberman, D. (2021). Histone H1 prevents non-CG
    methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.72676">https://doi.org/10.7554/elife.72676</a>
  chicago: Choi, Jaemyung, David B Lyons, and Daniel Zilberman. “Histone H1 Prevents
    Non-CG Methylation-Mediated Small RNA Biogenesis in Arabidopsis Heterochromatin.”
    <i>ELife</i>. eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/elife.72676">https://doi.org/10.7554/elife.72676</a>.
  ieee: J. Choi, D. B. Lyons, and D. Zilberman, “Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin,” <i>eLife</i>, vol. 10. eLife
    Sciences Publications, 2021.
  ista: Choi J, Lyons DB, Zilberman D. 2021. Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin. eLife. 10, e72676.
  mla: Choi, Jaemyung, et al. “Histone H1 Prevents Non-CG Methylation-Mediated Small
    RNA Biogenesis in Arabidopsis Heterochromatin.” <i>ELife</i>, vol. 10, e72676,
    eLife Sciences Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.72676">10.7554/elife.72676</a>.
  short: J. Choi, D.B. Lyons, D. Zilberman, ELife 10 (2021).
corr_author: '1'
date_created: 2021-12-10T13:12:08Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2025-04-14T07:57:42Z
day: '01'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.7554/elife.72676
ec_funded: 1
external_id:
  isi:
  - '000754832000001'
  pmid:
  - '34850679'
file:
- access_level: open_access
  checksum: 22ed4c55fb550f6da02ae55c359be651
  content_type: application/pdf
  creator: dernst
  date_created: 2022-05-16T10:42:22Z
  date_updated: 2022-05-16T10:42:22Z
  file_id: '11384'
  file_name: 2021_eLife_Choi.pdf
  file_size: 2715200
  relation: main_file
  success: 1
file_date_updated: 2022-05-16T10:42:22Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- genetics and molecular biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 62935a00-2b32-11ec-9570-eff30fa39068
  call_identifier: H2020
  grant_number: '725746'
  name: Quantitative analysis of DNA methylation maintenance with chromatin
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis
  heterochromatin
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '8997'
abstract:
- lang: eng
  text: Phenomenological relations such as Ohm’s or Fourier’s law have a venerable
    history in physics but are still scarce in biology. This situation restrains predictive
    theory. Here, we build on bacterial “growth laws,” which capture physiological
    feedback between translation and cell growth, to construct a minimal biophysical
    model for the combined action of ribosome-targeting antibiotics. Our model predicts
    drug interactions like antagonism or synergy solely from responses to individual
    drugs. We provide analytical results for limiting cases, which agree well with
    numerical results. We systematically refine the model by including direct physical
    interactions of different antibiotics on the ribosome. In a limiting case, our
    model provides a mechanistic underpinning for recent predictions of higher-order
    interactions that were derived using entropy maximization. We further refine the
    model to include the effects of antibiotics that mimic starvation and the presence
    of resistance genes. We describe the impact of a starvation-mimicking antibiotic
    on drug interactions analytically and verify it experimentally. Our extended model
    suggests a change in the type of drug interaction that depends on the strength
    of resistance, which challenges established rescaling paradigms. We experimentally
    show that the presence of unregulated resistance genes can lead to altered drug
    interaction, which agrees with the prediction of the model. While minimal, the
    model is readily adaptable and opens the door to predicting interactions of second
    and higher-order in a broad range of biological systems.
acknowledgement: 'This work was supported in part by Tum stipend of Knafelj foundation
  (to B.K.), Austrian Science Fund (FWF) standalone grants P 27201-B22 (to T.B.) and
  P 28844(to G.T.), HFSP program Grant RGP0042/2013 (to T.B.), German Research Foundation
  (DFG) individual grant BO 3502/2-1 (to T.B.), and German Research Foundation (DFG)
  Collaborative Research Centre (SFB) 1310 (to T.B.). '
article_number: e1008529
article_processing_charge: Yes
article_type: original
author:
- first_name: Bor
  full_name: Kavcic, Bor
  id: 350F91D2-F248-11E8-B48F-1D18A9856A87
  last_name: Kavcic
  orcid: 0000-0001-6041-254X
- first_name: Gašper
  full_name: Tkačik, Gašper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkačik
  orcid: 0000-0002-6699-1455
- first_name: Tobias
  full_name: Bollenbach, Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
citation:
  ama: Kavcic B, Tkačik G, Bollenbach MT. Minimal biophysical model of combined antibiotic
    action. <i>PLOS Computational Biology</i>. 2021;17. doi:<a href="https://doi.org/10.1371/journal.pcbi.1008529">10.1371/journal.pcbi.1008529</a>
  apa: Kavcic, B., Tkačik, G., &#38; Bollenbach, M. T. (2021). Minimal biophysical
    model of combined antibiotic action. <i>PLOS Computational Biology</i>. Public
    Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1008529">https://doi.org/10.1371/journal.pcbi.1008529</a>
  chicago: Kavcic, Bor, Gašper Tkačik, and Mark Tobias Bollenbach. “Minimal Biophysical
    Model of Combined Antibiotic Action.” <i>PLOS Computational Biology</i>. Public
    Library of Science, 2021. <a href="https://doi.org/10.1371/journal.pcbi.1008529">https://doi.org/10.1371/journal.pcbi.1008529</a>.
  ieee: B. Kavcic, G. Tkačik, and M. T. Bollenbach, “Minimal biophysical model of
    combined antibiotic action,” <i>PLOS Computational Biology</i>, vol. 17. Public
    Library of Science, 2021.
  ista: Kavcic B, Tkačik G, Bollenbach MT. 2021. Minimal biophysical model of combined
    antibiotic action. PLOS Computational Biology. 17, e1008529.
  mla: Kavcic, Bor, et al. “Minimal Biophysical Model of Combined Antibiotic Action.”
    <i>PLOS Computational Biology</i>, vol. 17, e1008529, Public Library of Science,
    2021, doi:<a href="https://doi.org/10.1371/journal.pcbi.1008529">10.1371/journal.pcbi.1008529</a>.
  short: B. Kavcic, G. Tkačik, M.T. Bollenbach, PLOS Computational Biology 17 (2021).
date_created: 2021-01-08T07:16:18Z
date_published: 2021-01-07T00:00:00Z
date_updated: 2025-06-12T06:33:18Z
day: '07'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1008529
external_id:
  isi:
  - '000608045000010'
  pmid:
  - '33411759'
file:
- access_level: open_access
  checksum: e29f2b42651bef8e034781de8781ffac
  content_type: application/pdf
  creator: dernst
  date_created: 2021-02-04T12:30:48Z
  date_updated: 2021-02-04T12:30:48Z
  file_id: '9092'
  file_name: 2021_PlosComBio_Kavcic.pdf
  file_size: 3690053
  relation: main_file
  success: 1
file_date_updated: 2021-02-04T12:30:48Z
has_accepted_license: '1'
intvolume: '        17'
isi: 1
keyword:
- Modelling and Simulation
- Genetics
- Molecular Biology
- Antibiotics
- Drug interactions
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P27201-B22
  name: Revealing the mechanisms underlying drug interactions
- _id: 254E9036-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P28844-B27
  name: Biophysics of information processing in gene regulation
publication: PLOS Computational Biology
publication_identifier:
  issn:
  - 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
  record:
  - id: '8930'
    relation: research_data
    status: public
  - id: '7673'
    relation: earlier_version
    status: public
scopus_import: '1'
status: public
title: Minimal biophysical model of combined antibiotic action
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2021'
...
---
_id: '9283'
abstract:
- lang: eng
  text: Gene expression levels are influenced by multiple coexisting molecular mechanisms.
    Some of these interactions such as those of transcription factors and promoters
    have been studied extensively. However, predicting phenotypes of gene regulatory
    networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic
    GRN to study in Escherichia coli how network phenotypes depend on local genetic
    context, i.e. the genetic neighborhood of a transcription factor and its relative
    position. We show that one GRN with fixed topology can display not only quantitatively
    but also qualitatively different phenotypes, depending solely on the local genetic
    context of its components. Transcriptional read-through is the main molecular
    mechanism that places one transcriptional unit (TU) within two separate regulons
    without the need for complex regulatory sequences. We propose that relative order
    of individual TUs, with its potential for combinatorial complexity, plays an important
    role in shaping phenotypes of GRNs.
acknowledgement: "We thank J Bollback, L Hurst, M Lagator, C Nizak, O Rivoire, M Savageau,
  G Tkacik, and B Vicozo\r\nfor helpful discussions; A Dolinar and A Greshnova for
  technical assistance; T Bollenbach for supplying the strain JW0336; C Rusnac, and
  members of the Guet lab for comments. The research leading to these results has
  received funding from the People Programme (Marie Curie Actions) of the European
  Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement n˚\r\n628377
  (ANS) and an Austrian Science Fund (FWF) grant n˚ I 3901-B32 (CCG)."
article_number: e65993
article_processing_charge: Yes
article_type: original
author:
- first_name: Anna A
  full_name: Nagy-Staron, Anna A
  id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
  last_name: Nagy-Staron
  orcid: 0000-0002-1391-8377
- first_name: Kathrin
  full_name: Tomasek, Kathrin
  id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
  last_name: Tomasek
  orcid: 0000-0003-3768-877X
- first_name: Caroline
  full_name: Caruso Carter, Caroline
  last_name: Caruso Carter
- first_name: Elisabeth
  full_name: Sonnleitner, Elisabeth
  last_name: Sonnleitner
- first_name: Bor
  full_name: Kavcic, Bor
  id: 350F91D2-F248-11E8-B48F-1D18A9856A87
  last_name: Kavcic
  orcid: 0000-0001-6041-254X
- first_name: Tiago
  full_name: Paixão, Tiago
  last_name: Paixão
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Nagy-Staron AA, Tomasek K, Caruso Carter C, et al. Local genetic context shapes
    the function of a gene regulatory network. <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/elife.65993">10.7554/elife.65993</a>
  apa: Nagy-Staron, A. A., Tomasek, K., Caruso Carter, C., Sonnleitner, E., Kavcic,
    B., Paixão, T., &#38; Guet, C. C. (2021). Local genetic context shapes the function
    of a gene regulatory network. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.65993">https://doi.org/10.7554/elife.65993</a>
  chicago: Nagy-Staron, Anna A, Kathrin Tomasek, Caroline Caruso Carter, Elisabeth
    Sonnleitner, Bor Kavcic, Tiago Paixão, and Calin C Guet. “Local Genetic Context
    Shapes the Function of a Gene Regulatory Network.” <i>ELife</i>. eLife Sciences
    Publications, 2021. <a href="https://doi.org/10.7554/elife.65993">https://doi.org/10.7554/elife.65993</a>.
  ieee: A. A. Nagy-Staron <i>et al.</i>, “Local genetic context shapes the function
    of a gene regulatory network,” <i>eLife</i>, vol. 10. eLife Sciences Publications,
    2021.
  ista: Nagy-Staron AA, Tomasek K, Caruso Carter C, Sonnleitner E, Kavcic B, Paixão
    T, Guet CC. 2021. Local genetic context shapes the function of a gene regulatory
    network. eLife. 10, e65993.
  mla: Nagy-Staron, Anna A., et al. “Local Genetic Context Shapes the Function of
    a Gene Regulatory Network.” <i>ELife</i>, vol. 10, e65993, eLife Sciences Publications,
    2021, doi:<a href="https://doi.org/10.7554/elife.65993">10.7554/elife.65993</a>.
  short: A.A. Nagy-Staron, K. Tomasek, C. Caruso Carter, E. Sonnleitner, B. Kavcic,
    T. Paixão, C.C. Guet, ELife 10 (2021).
corr_author: '1'
date_created: 2021-03-23T10:11:46Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2025-06-12T06:36:17Z
day: '08'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.7554/elife.65993
ec_funded: 1
external_id:
  isi:
  - '000631050900001'
  pmid:
  - '33683203'
file:
- access_level: open_access
  checksum: 3c2f44058c2dd45a5a1027f09d263f8e
  content_type: application/pdf
  creator: bkavcic
  date_created: 2021-03-23T10:12:58Z
  date_updated: 2021-03-23T10:12:58Z
  file_id: '9284'
  file_name: elife-65993-v2.pdf
  file_size: 1390469
  relation: main_file
  success: 1
file_date_updated: 2021-03-23T10:12:58Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- Genetics and Molecular Biology
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2517526A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '628377'
  name: 'The Systems Biology of Transcriptional Read-Through in Bacteria: from Synthetic
    Networks to Genomic Studies'
- _id: 268BFA92-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I03901
  name: Cybergenetic circuits to test composability of gene networks
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
  record:
  - id: '8951'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Local genetic context shapes the function of a gene regulatory network
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2021'
...
---
_id: '9387'
abstract:
- lang: eng
  text: We report the complete analysis of a deterministic model of deleterious mutations
    and negative selection against them at two haploid loci without recombination.
    As long as mutation is a weaker force than selection, mutant alleles remain rare
    at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
    If the mutation-free genotype is absent, generally the only stable equilibrium
    is the one that corresponds to fixation of the mutant allele at the locus where
    it is less deleterious. This result suggests that fixation of a deleterious allele
    that follows a click of the Muller’s ratchet is governed by natural selection,
    instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
  16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
  full_name: Khudiakova, Kseniia
  id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
  last_name: Khudiakova
  orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
  full_name: Neretina, Tatiana Yu.
  last_name: Neretina
- first_name: Alexey S.
  full_name: Kondrashov, Alexey S.
  last_name: Kondrashov
citation:
  ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
    balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. 2021;524.
    doi:<a href="https://doi.org/10.1016/j.jtbi.2021.110729">10.1016/j.jtbi.2021.110729</a>
  apa: Khudiakova, K., Neretina, T. Y., &#38; Kondrashov, A. S. (2021). Two linked
    loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical
    Biology</i>. Elsevier . <a href="https://doi.org/10.1016/j.jtbi.2021.110729">https://doi.org/10.1016/j.jtbi.2021.110729</a>
  chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
    Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal
    of Theoretical Biology</i>. Elsevier , 2021. <a href="https://doi.org/10.1016/j.jtbi.2021.110729">https://doi.org/10.1016/j.jtbi.2021.110729</a>.
  ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
    mutation-selection balance and Muller’s ratchet,” <i>Journal of Theoretical Biology</i>,
    vol. 524. Elsevier , 2021.
  ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
    balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
  mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
    and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>, vol. 524, 110729,
    Elsevier , 2021, doi:<a href="https://doi.org/10.1016/j.jtbi.2021.110729">10.1016/j.jtbi.2021.110729</a>.
  short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
    524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2025-06-12T06:40:55Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
  isi:
  - '000659161500002'
  pmid:
  - '33901507'
intvolume: '       524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
pmid: 1
publication: Journal of Theoretical Biology
publication_identifier:
  issn:
  - 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 524
year: '2021'
...
---
_id: '9431'
abstract:
- lang: eng
  text: Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report
    here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus
    from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid
    protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces
    infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram
    averaging, mature capsid-like particles show an IP6-like density in the CA hexamer,
    coordinated by rings of six lysines and six arginines. Phosphate and IP6 have
    opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons
    and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer
    formation. Subtomogram averaging and classification optimized for analysis of
    pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA
    polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast,
    the CA pentamer forms rigid units organizing the local architecture. These different
    features of hexamers and pentamers determine the structural mechanism to form
    CA polyhedrons of variable shape in mature RSV particles.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: EM-Fac
acknowledgement: This work was funded by the National Institute of Allergy and Infectious
  Diseases under awards R01AI147890 to R.A.D., R01AI150454 to V.M.V, R35GM136258 in
  support of J-P.R.F, and the Austrian Science Fund (FWF) grant P31445 to F.K.M.S.
  Access to high-resolution cryo-ET data acquisition at EMBL Heidelberg was supported
  by iNEXT (grant no. 653706), funded by the Horizon 2020 program of the European
  Union (PID 4246). We thank Wim Hagen and Felix Weis at EMBL Heidelberg for support
  in cryo-ET data acquisition. This work made use of the Cornell Center for Materials
  Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-179875).
  This research was also supported by the Scientific Service Units (SSUs) of IST Austria
  through resources provided by Scientific Computing (SciComp), the Life Science Facility
  (LSF), and the Electron Microscopy Facility (EMF).
article_number: '3226'
article_processing_charge: No
article_type: original
author:
- first_name: Martin
  full_name: Obr, Martin
  id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
  last_name: Obr
  orcid: 0000-0003-1756-6564
- first_name: Clifton L.
  full_name: Ricana, Clifton L.
  last_name: Ricana
- first_name: Nadia
  full_name: Nikulin, Nadia
  last_name: Nikulin
- first_name: Jon-Philip R.
  full_name: Feathers, Jon-Philip R.
  last_name: Feathers
- first_name: Marco
  full_name: Klanschnig, Marco
  last_name: Klanschnig
- first_name: Andreas
  full_name: Thader, Andreas
  id: 3A18A7B8-F248-11E8-B48F-1D18A9856A87
  last_name: Thader
- first_name: Marc C.
  full_name: Johnson, Marc C.
  last_name: Johnson
- first_name: Volker M.
  full_name: Vogt, Volker M.
  last_name: Vogt
- first_name: Florian KM
  full_name: Schur, Florian KM
  id: 48AD8942-F248-11E8-B48F-1D18A9856A87
  last_name: Schur
  orcid: 0000-0003-4790-8078
- first_name: Robert A.
  full_name: Dick, Robert A.
  last_name: Dick
citation:
  ama: Obr M, Ricana CL, Nikulin N, et al. Structure of the mature Rous sarcoma virus
    lattice reveals a role for IP6 in the formation of the capsid hexamer. <i>Nature
    Communications</i>. 2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23506-0">10.1038/s41467-021-23506-0</a>
  apa: Obr, M., Ricana, C. L., Nikulin, N., Feathers, J.-P. R., Klanschnig, M., Thader,
    A., … Dick, R. A. (2021). Structure of the mature Rous sarcoma virus lattice reveals
    a role for IP6 in the formation of the capsid hexamer. <i>Nature Communications</i>.
    Nature Research. <a href="https://doi.org/10.1038/s41467-021-23506-0">https://doi.org/10.1038/s41467-021-23506-0</a>
  chicago: Obr, Martin, Clifton L. Ricana, Nadia Nikulin, Jon-Philip R. Feathers,
    Marco Klanschnig, Andreas Thader, Marc C. Johnson, Volker M. Vogt, Florian KM
    Schur, and Robert A. Dick. “Structure of the Mature Rous Sarcoma Virus Lattice
    Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>.
    Nature Research, 2021. <a href="https://doi.org/10.1038/s41467-021-23506-0">https://doi.org/10.1038/s41467-021-23506-0</a>.
  ieee: M. Obr <i>et al.</i>, “Structure of the mature Rous sarcoma virus lattice
    reveals a role for IP6 in the formation of the capsid hexamer,” <i>Nature Communications</i>,
    vol. 12, no. 1. Nature Research, 2021.
  ista: Obr M, Ricana CL, Nikulin N, Feathers J-PR, Klanschnig M, Thader A, Johnson
    MC, Vogt VM, Schur FK, Dick RA. 2021. Structure of the mature Rous sarcoma virus
    lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
    Communications. 12(1), 3226.
  mla: Obr, Martin, et al. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals
    a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>,
    vol. 12, no. 1, 3226, Nature Research, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23506-0">10.1038/s41467-021-23506-0</a>.
  short: M. Obr, C.L. Ricana, N. Nikulin, J.-P.R. Feathers, M. Klanschnig, A. Thader,
    M.C. Johnson, V.M. Vogt, F.K. Schur, R.A. Dick, Nature Communications 12 (2021).
corr_author: '1'
date_created: 2021-05-28T14:25:50Z
date_published: 2021-05-28T00:00:00Z
date_updated: 2025-04-15T08:24:49Z
day: '28'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1038/s41467-021-23506-0
external_id:
  isi:
  - '000659145000011'
file:
- access_level: open_access
  checksum: 53ccc53d09a9111143839dbe7784e663
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-06-09T15:21:14Z
  date_updated: 2021-06-09T15:21:14Z
  file_id: '9538'
  file_name: 2021_NatureCommunications_Obr.pdf
  file_size: 6166295
  relation: main_file
  success: 1
file_date_updated: 2021-06-09T15:21:14Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 26736D6A-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P31445
  name: Structural conservation and diversity in retroviral capsid
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Nature Research
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/how-retroviruses-become-infectious/
scopus_import: '1'
status: public
title: Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in
  the formation of the capsid hexamer
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9540'
abstract:
- lang: eng
  text: The hexameric AAA-ATPase Drg1 is a key factor in eukaryotic ribosome biogenesis
    and initiates cytoplasmic maturation of the large ribosomal subunit by releasing
    the shuttling maturation factor Rlp24. Drg1 monomers contain two AAA-domains (D1
    and D2) that act in a concerted manner. Rlp24 release is inhibited by the drug
    diazaborine which blocks ATP hydrolysis in D2. The mode of inhibition was unknown.
    Here we show the first cryo-EM structure of Drg1 revealing the inhibitory mechanism.
    Diazaborine forms a covalent bond to the 2′-OH of the nucleotide in D2, explaining
    its specificity for this site. As a consequence, the D2 domain is locked in a
    rigid, inactive state, stalling the whole Drg1 hexamer. Resistance mechanisms
    identified include abolished drug binding and altered positioning of the nucleotide.
    Our results suggest nucleotide-modifying compounds as potential novel inhibitors
    for AAA-ATPases.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: We are deeply grateful to the late Gregor Högenauer who built the
  foundation for this study with his visionary work on the inhibitor diazaborine and
  its bacterial target. We thank Rolf Breinbauer for insightful discussions on boron
  chemistry. We thank Anton Meinhart and Tim Clausen for the valuable discussion of
  the manuscript. We are indebted to Thomas Köcher for the MS measurement of the diazaborine-ATPγS
  adduct. We thank the team of the VBCF for support during early phases of this work
  and the IST Austria Electron Microscopy Facility for providing equipment. The lab
  of D.H. is supported by Boehringer Ingelheim. The work was funded by FWF projects
  P32536 and P32977 (to H.B.).
article_number: '3483'
article_processing_charge: No
article_type: original
author:
- first_name: Michael
  full_name: Prattes, Michael
  last_name: Prattes
- first_name: Irina
  full_name: Grishkovskaya, Irina
  last_name: Grishkovskaya
- first_name: Victor-Valentin
  full_name: Hodirnau, Victor-Valentin
  id: 3661B498-F248-11E8-B48F-1D18A9856A87
  last_name: Hodirnau
  orcid: 0000-0003-3904-947X
- first_name: Ingrid
  full_name: Rössler, Ingrid
  last_name: Rössler
- first_name: Isabella
  full_name: Klein, Isabella
  last_name: Klein
- first_name: Christina
  full_name: Hetzmannseder, Christina
  last_name: Hetzmannseder
- first_name: Gertrude
  full_name: Zisser, Gertrude
  last_name: Zisser
- first_name: Christian C.
  full_name: Gruber, Christian C.
  last_name: Gruber
- first_name: Karl
  full_name: Gruber, Karl
  last_name: Gruber
- first_name: David
  full_name: Haselbach, David
  last_name: Haselbach
- first_name: Helmut
  full_name: Bergler, Helmut
  last_name: Bergler
citation:
  ama: Prattes M, Grishkovskaya I, Hodirnau V-V, et al. Structural basis for inhibition
    of the AAA-ATPase Drg1 by diazaborine. <i>Nature Communications</i>. 2021;12(1).
    doi:<a href="https://doi.org/10.1038/s41467-021-23854-x">10.1038/s41467-021-23854-x</a>
  apa: Prattes, M., Grishkovskaya, I., Hodirnau, V.-V., Rössler, I., Klein, I., Hetzmannseder,
    C., … Bergler, H. (2021). Structural basis for inhibition of the AAA-ATPase Drg1
    by diazaborine. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-021-23854-x">https://doi.org/10.1038/s41467-021-23854-x</a>
  chicago: Prattes, Michael, Irina Grishkovskaya, Victor-Valentin Hodirnau, Ingrid
    Rössler, Isabella Klein, Christina Hetzmannseder, Gertrude Zisser, et al. “Structural
    Basis for Inhibition of the AAA-ATPase Drg1 by Diazaborine.” <i>Nature Communications</i>.
    Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-23854-x">https://doi.org/10.1038/s41467-021-23854-x</a>.
  ieee: M. Prattes <i>et al.</i>, “Structural basis for inhibition of the AAA-ATPase
    Drg1 by diazaborine,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature,
    2021.
  ista: Prattes M, Grishkovskaya I, Hodirnau V-V, Rössler I, Klein I, Hetzmannseder
    C, Zisser G, Gruber CC, Gruber K, Haselbach D, Bergler H. 2021. Structural basis
    for inhibition of the AAA-ATPase Drg1 by diazaborine. Nature Communications. 12(1),
    3483.
  mla: Prattes, Michael, et al. “Structural Basis for Inhibition of the AAA-ATPase
    Drg1 by Diazaborine.” <i>Nature Communications</i>, vol. 12, no. 1, 3483, Springer
    Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23854-x">10.1038/s41467-021-23854-x</a>.
  short: M. Prattes, I. Grishkovskaya, V.-V. Hodirnau, I. Rössler, I. Klein, C. Hetzmannseder,
    G. Zisser, C.C. Gruber, K. Gruber, D. Haselbach, H. Bergler, Nature Communications
    12 (2021).
date_created: 2021-06-10T14:57:45Z
date_published: 2021-06-09T00:00:00Z
date_updated: 2024-10-21T06:02:01Z
day: '09'
ddc:
- '570'
department:
- _id: EM-Fac
doi: 10.1038/s41467-021-23854-x
external_id:
  isi:
  - '000664874700014'
  pmid:
  - '34108481'
file:
- access_level: open_access
  checksum: 40fc24c1310930990b52a8ad1142ee97
  content_type: application/pdf
  creator: cziletti
  date_created: 2021-06-15T18:55:59Z
  date_updated: 2021-06-15T18:55:59Z
  file_id: '9556'
  file_name: 2021_NatureComm_Prattes.pdf
  file_size: 3397292
  relation: main_file
  success: 1
file_date_updated: 2021-06-15T18:55:59Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Structural basis for inhibition of the AAA-ATPase Drg1 by diazaborine
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
OA_place: publisher
OA_type: gold
_id: '9778'
abstract:
- lang: eng
  text: The hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit.
    Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this
    synaptic connection. It is widely believed that mossy fiber PTP is an entirely
    presynaptic phenomenon, implying that PTP induction is input-specific, and requires
    neither activity of multiple inputs nor stimulation of postsynaptic neurons. To
    directly test cooperativity and associativity, we made paired recordings between
    single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain
    slices. By stimulating non-overlapping mossy fiber inputs converging onto single
    CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly,
    mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only
    minimal PTP after combined pre- and postsynaptic high-frequency stimulation with
    intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic
    spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP
    is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels,
    group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde
    vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire
    of synaptic computations, implementing a brake on mossy fiber detonation and a
    “smart teacher” function of hippocampal mossy fiber synapses.
acknowledged_ssus:
- _id: SSU
acknowledgement: We thank Drs. Carolina Borges-Merjane and Jose Guzman for critically
  reading the manuscript, and Pablo Castillo for discussions. We are grateful to Alois
  Schlögl for help with analysis, Florian Marr for excellent technical assistance
  and cell reconstruction, Christina Altmutter for technical help, Eleftheria Kralli-Beller
  for manuscript editing, and the Scientific Service Units of IST Austria for support.
  This project received funding from the European Research Council (ERC) under the
  European Union’s Horizon 2020 research and innovation program (grant agreement No
  692692) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27,
  Wittgenstein award), both to P.J.
article_number: '2912'
article_processing_charge: Yes
article_type: original
author:
- first_name: David H
  full_name: Vandael, David H
  id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
  last_name: Vandael
  orcid: 0000-0001-7577-1676
- first_name: Yuji
  full_name: Okamoto, Yuji
  id: 3337E116-F248-11E8-B48F-1D18A9856A87
  last_name: Okamoto
  orcid: 0000-0003-0408-6094
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Vandael DH, Okamoto Y, Jonas PM. Transsynaptic modulation of presynaptic short-term
    plasticity in hippocampal mossy fiber synapses. <i>Nature Communications</i>.
    2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23153-5">10.1038/s41467-021-23153-5</a>
  apa: Vandael, D. H., Okamoto, Y., &#38; Jonas, P. M. (2021). Transsynaptic modulation
    of presynaptic short-term plasticity in hippocampal mossy fiber synapses. <i>Nature
    Communications</i>. Springer. <a href="https://doi.org/10.1038/s41467-021-23153-5">https://doi.org/10.1038/s41467-021-23153-5</a>
  chicago: Vandael, David H, Yuji Okamoto, and Peter M Jonas. “Transsynaptic Modulation
    of Presynaptic Short-Term Plasticity in Hippocampal Mossy Fiber Synapses.” <i>Nature
    Communications</i>. Springer, 2021. <a href="https://doi.org/10.1038/s41467-021-23153-5">https://doi.org/10.1038/s41467-021-23153-5</a>.
  ieee: D. H. Vandael, Y. Okamoto, and P. M. Jonas, “Transsynaptic modulation of presynaptic
    short-term plasticity in hippocampal mossy fiber synapses,” <i>Nature Communications</i>,
    vol. 12, no. 1. Springer, 2021.
  ista: Vandael DH, Okamoto Y, Jonas PM. 2021. Transsynaptic modulation of presynaptic
    short-term plasticity in hippocampal mossy fiber synapses. Nature Communications.
    12(1), 2912.
  mla: Vandael, David H., et al. “Transsynaptic Modulation of Presynaptic Short-Term
    Plasticity in Hippocampal Mossy Fiber Synapses.” <i>Nature Communications</i>,
    vol. 12, no. 1, 2912, Springer, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23153-5">10.1038/s41467-021-23153-5</a>.
  short: D.H. Vandael, Y. Okamoto, P.M. Jonas, Nature Communications 12 (2021).
corr_author: '1'
date_created: 2021-08-06T07:22:55Z
date_published: 2021-05-18T00:00:00Z
date_updated: 2025-06-12T06:28:45Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/s41467-021-23153-5
ec_funded: 1
external_id:
  isi:
  - '000655481800014'
  pmid:
  - '34006874'
file:
- access_level: open_access
  checksum: 6036a8cdae95e1707c2a04d54e325ff4
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-12-17T11:34:50Z
  date_updated: 2021-12-17T11:34:50Z
  file_id: '10563'
  file_name: 2021_NatureCommunications_Vandael.pdf
  file_size: 3108845
  relation: main_file
  success: 1
file_date_updated: 2021-12-17T11:34:50Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '692692'
  name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Z00312
  name: Synaptic communication in neuronal microcircuits
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/synaptic-transmission-not-a-one-way-street/
scopus_import: '1'
status: public
title: Transsynaptic modulation of presynaptic short-term plasticity in hippocampal
  mossy fiber synapses
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2021'
...
---
_id: '8966'
abstract:
- lang: eng
  text: During development, a single cell is transformed into a highly complex organism
    through progressive cell division, specification and rearrangement. An important
    prerequisite for the emergence of patterns within the developing organism is to
    establish asymmetries at various scales, ranging from individual cells to the
    entire embryo, eventually giving rise to the different body structures. This becomes
    especially apparent during gastrulation, when the earliest major lineage restriction
    events lead to the formation of the different germ layers. Traditionally, the
    unfolding of the developmental program from symmetry breaking to germ layer formation
    has been studied by dissecting the contributions of different signaling pathways
    and cellular rearrangements in the in vivo context of intact embryos. Recent efforts,
    using the intrinsic capacity of embryonic stem cells to self-assemble and generate
    embryo-like structures de novo, have opened new avenues for understanding the
    many ways by which an embryo can be built and the influence of extrinsic factors
    therein. Here, we discuss and compare divergent and conserved strategies leading
    to germ layer formation in embryos as compared to in vitro systems, their upstream
    molecular cascades and the role of extrinsic factors in this process.
acknowledgement: We thank Nicoletta Petridou, Diana Pinheiro, Cornelia Schwayer and
  Stefania Tavano for feedback on the manuscript. Research in the Heisenberg lab is
  supported by an ERC Advanced Grant (MECSPEC 742573) to C.-P.H. A.S. is a recipient
  of a DOC Fellowship of the Austrian Academy of Science.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Alexandra
  full_name: Schauer, Alexandra
  id: 30A536BA-F248-11E8-B48F-1D18A9856A87
  last_name: Schauer
  orcid: 0000-0001-7659-9142
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Schauer A, Heisenberg C-PJ. Reassembling gastrulation. <i>Developmental Biology</i>.
    2021;474:71-81. doi:<a href="https://doi.org/10.1016/j.ydbio.2020.12.014">10.1016/j.ydbio.2020.12.014</a>
  apa: Schauer, A., &#38; Heisenberg, C.-P. J. (2021). Reassembling gastrulation.
    <i>Developmental Biology</i>. Elsevier. <a href="https://doi.org/10.1016/j.ydbio.2020.12.014">https://doi.org/10.1016/j.ydbio.2020.12.014</a>
  chicago: Schauer, Alexandra, and Carl-Philipp J Heisenberg. “Reassembling Gastrulation.”
    <i>Developmental Biology</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.ydbio.2020.12.014">https://doi.org/10.1016/j.ydbio.2020.12.014</a>.
  ieee: A. Schauer and C.-P. J. Heisenberg, “Reassembling gastrulation,” <i>Developmental
    Biology</i>, vol. 474. Elsevier, pp. 71–81, 2021.
  ista: Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental
    Biology. 474, 71–81.
  mla: Schauer, Alexandra, and Carl-Philipp J. Heisenberg. “Reassembling Gastrulation.”
    <i>Developmental Biology</i>, vol. 474, Elsevier, 2021, pp. 71–81, doi:<a href="https://doi.org/10.1016/j.ydbio.2020.12.014">10.1016/j.ydbio.2020.12.014</a>.
  short: A. Schauer, C.-P.J. Heisenberg, Developmental Biology 474 (2021) 71–81.
date_created: 2020-12-22T09:53:34Z
date_published: 2021-06-01T00:00:00Z
date_updated: 2026-06-19T22:30:15Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.ydbio.2020.12.014
ec_funded: 1
external_id:
  isi:
  - '000639461800008'
  pmid:
  - '33352181'
file:
- access_level: open_access
  checksum: fa2a5731fd16ab171b029f32f031c440
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-08-11T10:28:06Z
  date_updated: 2021-08-11T10:28:06Z
  file_id: '9880'
  file_name: 2021_DevBiology_Schauer.pdf
  file_size: 1440321
  relation: main_file
  success: 1
file_date_updated: 2021-08-11T10:28:06Z
has_accepted_license: '1'
intvolume: '       474'
isi: 1
keyword:
- Developmental Biology
- Cell Biology
- Molecular Biology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 71-81
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742573'
  name: Interaction and feedback between cell mechanics and fate specification in
    vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
  grant_number: '25239'
  name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
publication: Developmental Biology
publication_identifier:
  issn:
  - 0012-1606
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
  record:
  - id: '12891'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Reassembling gastrulation
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 474
year: '2021'
...
---
_id: '9429'
abstract:
- lang: eng
  text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3
    lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency
    leads to motor coordination deficits as well as ASD-relevant social and cognitive
    impairments. However, induction of Cul3 haploinsufficiency later in life does
    not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during
    a critical developmental window. Here we show that Cul3 is essential to regulate
    neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice
    display cortical lamination abnormalities. At the molecular level, we found that
    Cul3 controls neuronal migration by tightly regulating the amount of Plastin3
    (Pls3), a previously unrecognized player of neural migration. Furthermore, we
    found that Pls3 cell-autonomously regulates cell migration by regulating actin
    cytoskeleton organization, and its levels are inversely proportional to neural
    migration speed. Finally, we provide evidence that cellular phenotypes associated
    with autism-linked gene haploinsufficiency can be rescued by transcriptional activation
    of the intact allele in vitro, offering a proof of concept for a potential therapeutic
    approach for ASDs.
acknowledged_ssus:
- _id: PreCl
acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A.
  Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the
  management of our animal colony, as well as M. Schunn and the Preclinical Facility
  team for technical assistance. We thank K. Heesom and her team at the University
  of Bristol Proteomics Facility for the proteomics sample preparation, data generation,
  and analysis support. We thank Y. B. Simon for kindly providing the plasmid for
  lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration
  and the fruitful discussions. This work was supported by the ISTPlus postdoctoral
  fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon
  2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by
  the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D
  (I3600-B27).
article_number: '3058'
article_processing_charge: No
article_type: original
author:
- first_name: Jasmin
  full_name: Morandell, Jasmin
  id: 4739D480-F248-11E8-B48F-1D18A9856A87
  last_name: Morandell
- first_name: Lena A
  full_name: Schwarz, Lena A
  id: 29A8453C-F248-11E8-B48F-1D18A9856A87
  last_name: Schwarz
- first_name: Bernadette
  full_name: Basilico, Bernadette
  id: 36035796-5ACA-11E9-A75E-7AF2E5697425
  last_name: Basilico
  orcid: 0000-0003-1843-3173
- first_name: Saren
  full_name: Tasciyan, Saren
  id: 4323B49C-F248-11E8-B48F-1D18A9856A87
  last_name: Tasciyan
  orcid: 0000-0003-1671-393X
- first_name: Georgi A
  full_name: Dimchev, Georgi A
  id: 38C393BE-F248-11E8-B48F-1D18A9856A87
  last_name: Dimchev
  orcid: 0000-0001-8370-6161
- first_name: Armel
  full_name: Nicolas, Armel
  id: 2A103192-F248-11E8-B48F-1D18A9856A87
  last_name: Nicolas
- first_name: Christoph M
  full_name: Sommer, Christoph M
  id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
  last_name: Sommer
  orcid: 0000-0003-1216-9105
- first_name: Caroline
  full_name: Kreuzinger, Caroline
  id: 382077BA-F248-11E8-B48F-1D18A9856A87
  last_name: Kreuzinger
- first_name: Christoph
  full_name: Dotter, Christoph
  id: 4C66542E-F248-11E8-B48F-1D18A9856A87
  last_name: Dotter
  orcid: 0000-0002-9033-9096
- first_name: Lisa
  full_name: Knaus, Lisa
  id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
  last_name: Knaus
- first_name: Zoe
  full_name: Dobler, Zoe
  id: D23090A2-9057-11EA-883A-A8396FC7A38F
  last_name: Dobler
- first_name: Emanuele
  full_name: Cacci, Emanuele
  last_name: Cacci
- first_name: Florian KM
  full_name: Schur, Florian KM
  id: 48AD8942-F248-11E8-B48F-1D18A9856A87
  last_name: Schur
  orcid: 0000-0003-4790-8078
- first_name: Johann G
  full_name: Danzl, Johann G
  id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
  last_name: Danzl
  orcid: 0000-0001-8559-3973
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
citation:
  ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein
    homeostasis and cell migration during a critical window of brain development.
    <i>Nature Communications</i>. 2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23123-x">10.1038/s41467-021-23123-x</a>
  apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A.,
    Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis
    and cell migration during a critical window of brain development. <i>Nature Communications</i>.
    Springer Nature. <a href="https://doi.org/10.1038/s41467-021-23123-x">https://doi.org/10.1038/s41467-021-23123-x</a>
  chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan,
    Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton
    Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.”
    <i>Nature Communications</i>. Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-23123-x">https://doi.org/10.1038/s41467-021-23123-x</a>.
  ieee: J. Morandell <i>et al.</i>, “Cul3 regulates cytoskeleton protein homeostasis
    and cell migration during a critical window of brain development,” <i>Nature Communications</i>,
    vol. 12, no. 1. Springer Nature, 2021.
  ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer
    CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino
    G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during
    a critical window of brain development. Nature Communications. 12(1), 3058.
  mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis
    and Cell Migration during a Critical Window of Brain Development.” <i>Nature Communications</i>,
    vol. 12, no. 1, 3058, Springer Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23123-x">10.1038/s41467-021-23123-x</a>.
  short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas,
    C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur,
    J.G. Danzl, G. Novarino, Nature Communications 12 (2021).
corr_author: '1'
date_created: 2021-05-28T11:49:46Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2026-06-19T22:31:00Z
day: '24'
ddc:
- '572'
department:
- _id: GaNo
- _id: JoDa
- _id: FlSc
- _id: MiSi
- _id: LifeSc
- _id: Bio
doi: 10.1038/s41467-021-23123-x
ec_funded: 1
external_id:
  isi:
  - '000658769900010'
file:
- access_level: open_access
  checksum: 337e0f7959c35ec959984cacdcb472ba
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-05-28T12:39:43Z
  date_updated: 2021-05-28T12:39:43Z
  file_id: '9430'
  file_name: 2021_NatureCommunications_Morandell.pdf
  file_size: 9358599
  relation: main_file
  success: 1
file_date_updated: 2021-05-28T12:39:43Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
- _id: 25444568-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715508'
  name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
    and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W1232
  name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
  grant_number: F7807
  name: Stem Cell Modulation in Neural Development and Regeneration/ P07-Neural stem
    cells in autism and epilepsy
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I03600
  name: Optical control of synaptic function via adhesion molecules
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  link:
  - relation: press_release
    url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/
  record:
  - id: '19557'
    relation: dissertation_contains
    status: public
  - id: '7800'
    relation: earlier_version
    status: public
  - id: '12401'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a
  critical window of brain development
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '12189'
abstract:
- lang: eng
  text: Meiotic crossovers (COs) are important for reshuffling genetic information
    between homologous chromosomes and they are essential for their correct segregation.
    COs are unevenly distributed along chromosomes and the underlying mechanisms controlling
    CO localization are not well understood. We previously showed that meiotic COs
    are mis-localized in the absence of AXR1, an enzyme involved in the neddylation/rubylation
    protein modification pathway in Arabidopsis thaliana. Here, we report that in
    axr1-/-, male meiocytes show a strong defect in chromosome pairing whereas the
    formation of the telomere bouquet is not affected. COs are also redistributed
    towards subtelomeric chromosomal ends where they frequently form clusters, in
    contrast to large central regions depleted in recombination. The CO suppressed
    regions correlate with DNA hypermethylation of transposable elements (TEs) in
    the CHH context in axr1-/- meiocytes. Through examining somatic methylomes, we
    found axr1-/- affects DNA methylation in a plant, causing hypermethylation in
    all sequence contexts (CG, CHG and CHH) in TEs. Impairment of the main pathways
    involved in DNA methylation is epistatic over axr1-/- for DNA methylation in somatic
    cells but does not restore regular chromosome segregation during meiosis. Collectively,
    our findings reveal that the neddylation pathway not only regulates hormonal perception
    and CO distribution but is also, directly or indirectly, a major limiting pathway
    of TE DNA methylation in somatic cells.
acknowledgement: The authors wish to thank Cécile Raynaud, Eric Jenczewski, Rajeev
  Kumar, Raphaël Mercier and Jean Molinier for critical reading of the manuscript.
article_number: e1008894
article_processing_charge: No
article_type: original
author:
- first_name: Nicolas
  full_name: Christophorou, Nicolas
  last_name: Christophorou
- first_name: Wenjing
  full_name: She, Wenjing
  last_name: She
- first_name: Jincheng
  full_name: Long, Jincheng
  last_name: Long
- first_name: Aurélie
  full_name: Hurel, Aurélie
  last_name: Hurel
- first_name: Sébastien
  full_name: Beaubiat, Sébastien
  last_name: Beaubiat
- first_name: Yassir
  full_name: Idir, Yassir
  last_name: Idir
- first_name: Marina
  full_name: Tagliaro-Jahns, Marina
  last_name: Tagliaro-Jahns
- first_name: Aurélie
  full_name: Chambon, Aurélie
  last_name: Chambon
- first_name: Victor
  full_name: Solier, Victor
  last_name: Solier
- first_name: Daniel
  full_name: Vezon, Daniel
  last_name: Vezon
- first_name: Mathilde
  full_name: Grelon, Mathilde
  last_name: Grelon
- first_name: Xiaoqi
  full_name: Feng, Xiaoqi
  id: e0164712-22ee-11ed-b12a-d80fcdf35958
  last_name: Feng
  orcid: 0000-0002-4008-1234
- first_name: Nicolas
  full_name: Bouché, Nicolas
  last_name: Bouché
- first_name: Christine
  full_name: Mézard, Christine
  last_name: Mézard
citation:
  ama: Christophorou N, She W, Long J, et al. AXR1 affects DNA methylation independently
    of its role in regulating meiotic crossover localization. <i>PLOS Genetics</i>.
    2020;16(6). doi:<a href="https://doi.org/10.1371/journal.pgen.1008894">10.1371/journal.pgen.1008894</a>
  apa: Christophorou, N., She, W., Long, J., Hurel, A., Beaubiat, S., Idir, Y., …
    Mézard, C. (2020). AXR1 affects DNA methylation independently of its role in regulating
    meiotic crossover localization. <i>PLOS Genetics</i>. Public Library of Science
    (PLoS). <a href="https://doi.org/10.1371/journal.pgen.1008894">https://doi.org/10.1371/journal.pgen.1008894</a>
  chicago: Christophorou, Nicolas, Wenjing She, Jincheng Long, Aurélie Hurel, Sébastien
    Beaubiat, Yassir Idir, Marina Tagliaro-Jahns, et al. “AXR1 Affects DNA Methylation
    Independently of Its Role in Regulating Meiotic Crossover Localization.” <i>PLOS
    Genetics</i>. Public Library of Science (PLoS), 2020. <a href="https://doi.org/10.1371/journal.pgen.1008894">https://doi.org/10.1371/journal.pgen.1008894</a>.
  ieee: N. Christophorou <i>et al.</i>, “AXR1 affects DNA methylation independently
    of its role in regulating meiotic crossover localization,” <i>PLOS Genetics</i>,
    vol. 16, no. 6. Public Library of Science (PLoS), 2020.
  ista: Christophorou N, She W, Long J, Hurel A, Beaubiat S, Idir Y, Tagliaro-Jahns
    M, Chambon A, Solier V, Vezon D, Grelon M, Feng X, Bouché N, Mézard C. 2020. AXR1
    affects DNA methylation independently of its role in regulating meiotic crossover
    localization. PLOS Genetics. 16(6), e1008894.
  mla: Christophorou, Nicolas, et al. “AXR1 Affects DNA Methylation Independently
    of Its Role in Regulating Meiotic Crossover Localization.” <i>PLOS Genetics</i>,
    vol. 16, no. 6, e1008894, Public Library of Science (PLoS), 2020, doi:<a href="https://doi.org/10.1371/journal.pgen.1008894">10.1371/journal.pgen.1008894</a>.
  short: N. Christophorou, W. She, J. Long, A. Hurel, S. Beaubiat, Y. Idir, M. Tagliaro-Jahns,
    A. Chambon, V. Solier, D. Vezon, M. Grelon, X. Feng, N. Bouché, C. Mézard, PLOS
    Genetics 16 (2020).
date_created: 2023-01-16T09:16:10Z
date_published: 2020-06-29T00:00:00Z
date_updated: 2023-05-08T10:54:39Z
day: '29'
department:
- _id: XiFe
doi: 10.1371/journal.pgen.1008894
extern: '1'
external_id:
  pmid:
  - '32598340'
intvolume: '        16'
issue: '6'
keyword:
- Cancer Research
- Genetics (clinical)
- Genetics
- Molecular Biology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7351236/
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
  issn:
  - 1553-7404
publication_status: published
publisher: Public Library of Science (PLoS)
quality_controlled: '1'
scopus_import: '1'
status: public
title: AXR1 affects DNA methylation independently of its role in regulating meiotic
  crossover localization
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2020'
...
