---
OA_place: publisher
_id: '6263'
abstract:
- lang: eng
  text: 'Antibiotic  resistance  can  emerge  spontaneously  through  genomic  mutation  and  render
    treatment   ineffective.   To   counteract   this process, in   addition   to   the   discovery   and
    description of resistance mechanisms,a deeper understanding of resistanceevolvabilityand
    its  determinantsis  needed. To address  this challenge,  this  thesisuncoversnew  genetic
    determinants   of   resistance   evolvability   using   a   customized   robotic   setup,
    exploressystematic   ways   in   which   resistance   evolution   is   perturbed   due   to
    dose-responsecharacteristics  of  drugs and  mutation  rate  differences,and  mathematically  investigates
    the evolutionary fate of one specific type of evolvability modifier -a stress-induced
    mutagenesis allele.We  find  severalgenes  which  strongly  inhibit  or  potentiate  resistance  evolution.  In  order
    to identify   them,   we   first developedan   automated   high-throughput   feedback-controlled
    protocol whichkeeps the population size and selection pressure approximately constant
    for hundreds  of  cultures  by  dynamically  re-diluting  the  cultures  and  adjusting  the  antibiotic
    concentration.  We  implementedthis  protocol  on  a  customized  liquid  handling  robot  and
    propagated  100  different  gene  deletion  strains  of Escherichia  coliin  triplicate  for  over  100
    generations  in  tetracycline  and  in  chloramphenicol,  and  comparedtheir  adaptation  rates.We  find  a  diminishing  returns  pattern,  where  initially  sensitive  strains  adapted  more
    compared to less sensitive ones.  Our data uncover that deletions of certain genes
    which do not  affect  mutation  rate,including  efflux  pump  components,  a  chaperone  and
    severalstructural  and regulatory  genes  can strongly  and  reproducibly  alterresistance  evolution.
    Sequencing   analysis of   evolved   populations   indicates   that   epistasis   with   resistance
    mutations  is  the  most  likelyexplanation. This  work  could  inspire  treatment  strategies  in
    which  targeted  inhibitors  of  evolvability  mechanisms  will  be  given  alongside  antibiotics  to
    slow down resistance evolution and extend theefficacy of antibiotics.We implemented  astochasticpopulation  genetics  model,
    toverifyways  in  which  general properties,  namely,  dose-response  characteristics  of  drugs  and  mutation  rates,  influence
    evolutionary  dynamics.  In  particular,  under  the  exposure  to  antibiotics  with  shallow  dose-response  curves,bacteria  have  narrower  distributions  of  fitness  effects  of  new  mutations.
    We  show  that in  silicothis  also  leads  to  slower  resistance  evolution.  We
    see and  confirm with experiments that increased mutation rates, apart from speeding
    up evolution, also leadto high reproducibility of phenotypic adaptation in a context
    of continually strong selection pressure.Knowledge  of  these  patterns  can  aid  in  predicting  the  dynamics  of  antibiotic
    resistance evolutionand adapting treatment schemes accordingly.Focusing on   a   previously   described   type   of   evolvability   modifier
    –a   stress-induced mutagenesis  allele –we  find  conditions  under  which  it  can  persist  in  a  population  under
    periodic  selectionakin  to  clinical  treatment. We  set  up  a  deterministic
    infinite  populationcontinuous  time  model  tracking  the  frequencies  of  a  mutator  and  resistance  allele  and
    evaluate  various  treatment  schemes  in  how  well  they  maintain  a stress-induced
    mutator allele. In particular,a high diversity  of stresses  is  crucial  for  the  persistence
    of the  mutator allele. This leads to a general trade-off where exactly those
    diversifying treatment schemes which  are  likely  to  decrease  levels  of  resistance  could  lead  to  stronger  selection  of  highly
    evolvable genotypes.In  the  long  run,  this  work  will  lead  to  a  deeper  understanding  of  the  genetic  and  cellular
    mechanisms involved in antibiotic resistance evolution and could inspire new strategies
    for slowing down its rate. '
acknowledged_ssus:
- _id: M-Shop
- _id: LifeSc
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Marta
  full_name: Lukacisinova, Marta
  id: 4342E402-F248-11E8-B48F-1D18A9856A87
  last_name: Lukacisinova
  orcid: 0000-0002-2519-8004
citation:
  ama: Lukacisinova M. Genetic determinants of antibiotic resistance evolution. 2018.
    doi:<a href="https://doi.org/10.15479/AT:ISTA:th1072">10.15479/AT:ISTA:th1072</a>
  apa: Lukacisinova, M. (2018). <i>Genetic determinants of antibiotic resistance evolution</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th1072">https://doi.org/10.15479/AT:ISTA:th1072</a>
  chicago: Lukacisinova, Marta. “Genetic Determinants of Antibiotic Resistance Evolution.”
    Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th1072">https://doi.org/10.15479/AT:ISTA:th1072</a>.
  ieee: M. Lukacisinova, “Genetic determinants of antibiotic resistance evolution,”
    Institute of Science and Technology Austria, 2018.
  ista: Lukacisinova M. 2018. Genetic determinants of antibiotic resistance evolution.
    Institute of Science and Technology Austria.
  mla: Lukacisinova, Marta. <i>Genetic Determinants of Antibiotic Resistance Evolution</i>.
    Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th1072">10.15479/AT:ISTA:th1072</a>.
  short: M. Lukacisinova, Genetic Determinants of Antibiotic Resistance Evolution,
    Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2019-04-09T13:57:15Z
date_published: 2018-12-28T00:00:00Z
date_updated: 2026-07-30T14:47:59Z
day: '28'
ddc:
- '570'
- '576'
- '579'
degree_awarded: PhD
department:
- _id: ToBo
- _id: GradSch
doi: 10.15479/AT:ISTA:th1072
doi_confirm: '1'
file:
- access_level: open_access
  checksum: fc60585c9eaad868ac007004ef130908
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  creator: dernst
  date_created: 2019-04-09T13:49:24Z
  date_updated: 2021-02-11T11:17:17Z
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  relation: main_file
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  content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
  creator: dernst
  date_created: 2019-04-09T13:49:23Z
  date_updated: 2020-07-14T12:47:25Z
  embargo_to: open_access
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file_date_updated: 2021-02-11T11:17:17Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th1072
has_accepted_license: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: '91'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '1027'
    relation: part_of_dissertation
    status: public
  - id: '696'
    relation: part_of_dissertation
    status: public
  - id: '1619'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Tobias
  full_name: Bollenbach, Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
title: Genetic determinants of antibiotic resistance evolution
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
_id: '612'
abstract:
- lang: eng
  text: Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically
    and postsynaptically through the modulation of different effector signalling pathways.
    Here, we analysed the distribution of GABAB receptors using highly sensitive SDS-digested
    freeze-fracture replica labelling in mouse cerebellar Purkinje cells. Immunoreactivity
    for GABAB1 was observed on presynaptic and, more abundantly, on postsynaptic compartments,
    showing both scattered and clustered distribution patterns. Quantitative analysis
    of immunoparticles revealed a somato-dendritic gradient, with the density of immunoparticles
    increasing 26-fold from somata to dendritic spines. To understand the spatial
    relationship of GABAB receptors with two key effector ion channels, the G protein-gated
    inwardly rectifying K+ (GIRK/Kir3) channel and the voltage-dependent Ca2+ channel,
    biochemical and immunohistochemical approaches were performed. Co-immunoprecipitation
    analysis demonstrated that GABAB receptors co-assembled with GIRK and CaV2.1 channels
    in the cerebellum. Using double-labelling immunoelectron microscopic techniques,
    co-clustering between GABAB1 and GIRK2 was detected in dendritic spines, whereas
    they were mainly segregated in the dendritic shafts. In contrast, co-clustering
    of GABAB1 and CaV2.1 was detected in dendritic shafts but not spines. Presynaptically,
    although no significant co-clustering of GABAB1 and GIRK2 or CaV2.1 channels was
    detected, inter-cluster distance for GABAB1 and GIRK2 was significantly smaller
    in the active zone than in the dendritic shafts, and that for GABAB1 and CaV2.1
    was significantly smaller in the active zone than in the dendritic shafts and
    spines. Thus, GABAB receptors are associated with GIRK and CaV2.1 channels in
    different subcellular compartments. These data provide a better framework for
    understanding the different roles played by GABAB receptors and their effector
    ion channels in the cerebellar network.
article_processing_charge: No
article_type: original
author:
- first_name: Rafael
  full_name: Luján, Rafael
  last_name: Luján
- first_name: Carolina
  full_name: Aguado, Carolina
  last_name: Aguado
- first_name: Francisco
  full_name: Ciruela, Francisco
  last_name: Ciruela
- first_name: Javier
  full_name: Cózar, Javier
  last_name: Cózar
- first_name: David
  full_name: Kleindienst, David
  id: 42E121A4-F248-11E8-B48F-1D18A9856A87
  last_name: Kleindienst
- first_name: Luis
  full_name: De La Ossa, Luis
  last_name: De La Ossa
- first_name: Bernhard
  full_name: Bettler, Bernhard
  last_name: Bettler
- first_name: Kevin
  full_name: Wickman, Kevin
  last_name: Wickman
- first_name: Masahiko
  full_name: Watanabe, Masahiko
  last_name: Watanabe
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Yugo
  full_name: Fukazawa, Yugo
  last_name: Fukazawa
citation:
  ama: Luján R, Aguado C, Ciruela F, et al. Differential association of GABAB receptors
    with their effector ion channels in Purkinje cells. <i>Brain Structure and Function</i>.
    2018;223(3):1565-1587. doi:<a href="https://doi.org/10.1007/s00429-017-1568-y">10.1007/s00429-017-1568-y</a>
  apa: Luján, R., Aguado, C., Ciruela, F., Cózar, J., Kleindienst, D., De La Ossa,
    L., … Fukazawa, Y. (2018). Differential association of GABAB receptors with their
    effector ion channels in Purkinje cells. <i>Brain Structure and Function</i>.
    Springer. <a href="https://doi.org/10.1007/s00429-017-1568-y">https://doi.org/10.1007/s00429-017-1568-y</a>
  chicago: Luján, Rafael, Carolina Aguado, Francisco Ciruela, Javier Cózar, David
    Kleindienst, Luis De La Ossa, Bernhard Bettler, et al. “Differential Association
    of GABAB Receptors with Their Effector Ion Channels in Purkinje Cells.” <i>Brain
    Structure and Function</i>. Springer, 2018. <a href="https://doi.org/10.1007/s00429-017-1568-y">https://doi.org/10.1007/s00429-017-1568-y</a>.
  ieee: R. Luján <i>et al.</i>, “Differential association of GABAB receptors with
    their effector ion channels in Purkinje cells,” <i>Brain Structure and Function</i>,
    vol. 223, no. 3. Springer, pp. 1565–1587, 2018.
  ista: Luján R, Aguado C, Ciruela F, Cózar J, Kleindienst D, De La Ossa L, Bettler
    B, Wickman K, Watanabe M, Shigemoto R, Fukazawa Y. 2018. Differential association
    of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure
    and Function. 223(3), 1565–1587.
  mla: Luján, Rafael, et al. “Differential Association of GABAB Receptors with Their
    Effector Ion Channels in Purkinje Cells.” <i>Brain Structure and Function</i>,
    vol. 223, no. 3, Springer, 2018, pp. 1565–87, doi:<a href="https://doi.org/10.1007/s00429-017-1568-y">10.1007/s00429-017-1568-y</a>.
  short: R. Luján, C. Aguado, F. Ciruela, J. Cózar, D. Kleindienst, L. De La Ossa,
    B. Bettler, K. Wickman, M. Watanabe, R. Shigemoto, Y. Fukazawa, Brain Structure
    and Function 223 (2018) 1565–1587.
date_created: 2018-12-11T11:47:29Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2026-10-06T22:31:02Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1007/s00429-017-1568-y
ec_funded: 1
external_id:
  isi:
  - '000428419500030'
file:
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  checksum: a55b3103476ecb5f4f983d8801807e8b
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:36Z
  date_updated: 2020-07-14T12:47:20Z
  file_id: '5157'
  file_name: IST-2018-1013-v1+1_2018_Kleindienst_Differential.pdf
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  relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
fulldoi: https://doi.org/10.1007/s00429-017-1568-y
has_accepted_license: '1'
intvolume: '       223'
isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '04'
oa: 1
oa_version: Published Version
page: 1565 - 1587
project:
- _id: 25CBA828-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '720270'
  name: Human Brain Project Specific Grant Agreement 1
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Brain Structure and Function
publication_status: published
publisher: Springer
publist_id: '7192'
pubrep_id: '1013'
quality_controlled: '1'
related_material:
  record:
  - id: '9562'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Differential association of GABAB receptors with their effector ion channels
  in Purkinje cells
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 223
year: '2018'
...
---
OA_place: publisher
_id: '51'
abstract:
- lang: eng
  text: Asymmetries have long been known about in the central nervous system. From
    gross anatomical differences, such as the presence of the parapineal organ in
    only one hemisphere of the developing zebrafish, to more subtle differences in
    activity between both hemispheres, as seen in freely roaming animals or human
    participants under PET and fMRI imaging analysis. The presence of asymmetries
    has been demonstrated to have huge behavioural implications, with their disruption
    often leading to the generation of neurological disorders, memory problems, changes
    in personality, and in an organism's health and well-being. For my Ph.D. work
    I aimed to tackle two important avenues of research. The first being the process
    of input-side dependency in the hippocampus, with the goal of finding a key gene
    responsible for its development (Gene X). The second project was to do with experience-induced
    laterality formation in the hippocampus. Specifically, how laterality in the synapse
    density of the CA1 stratum radiatum (s.r.) could be induced purely through environmental
    enrichment. Through unilateral tracer injections into the CA3, I was able to selectively
    measure the properties of synapses within the CA1 and investigate how they differed
    based upon which hemisphere the presynaptic neurone originated. Having found the
    existence of a previously unreported reversed (left-isomerism) i.v. mutant, through
    morpholocal examination of labelled terminals in the CA1 s.r., I aimed to elucidate
    a key gene responsible for the process of left or right determination of inputs
    to the CA1 s.r.. This work relates to the previous finding of input-side dependent
    asymmetry in the wild-type rodent, where the origin of the projecting neurone
    to the CA1 will determine the morphology of a synapse, to a greater degree than
    the hemisphere in which the projection terminates. Using left- and right-isomerism
    i.v. mice, in combination with whole genome sequence analysis, I highlight Ena/VASP-like
    (Evl) as a potential target for Gene X. In relation to this topic, I also highlight
    my work in the recently published paper of how knockout of PirB can lead to a
    lack of input-side dependency in the murine hippocampus. For the second question,
    I show that the environmental enrichment paradigm will lead to an asymmetry in
    the synapse densities in the hippocampus of mice. I also highlight that the nature
    of the enrichment is of less consequence than the process of enrichment itself.
    I demonstrate that the CA3 region will dramatically alter its projection targets,
    in relation to environmental stimulation, with the asymmetry in synaptic density,
    caused by enrichment, relying heavily on commissural fibres. I also highlight
    the vital importance of input-side dependent asymmetry, as a necessary component
    of experience-dependent laterality formation in the CA1 s.r.. However, my results
    suggest that it isn't the only cause, as there appears to be a CA1 dependent mechanism
    also at play. Upon further investigation, I highlight the significant, and highly
    important, finding that the changes seen in the CA1 s.r. were predominantly caused
    through projections from the left-CA3, with the right-CA3 having less involvement
    in this mechanism.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Matthew J
  full_name: Case, Matthew J
  id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
  last_name: Case
citation:
  ama: 'Case MJ. From the left to the right: A tale of asymmetries, environments,
    and hippocampal development. 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th_1032">10.15479/AT:ISTA:th_1032</a>'
  apa: 'Case, M. J. (2018). <i>From the left to the right: A tale of asymmetries,
    environments, and hippocampal development</i>. Institute of Science and Technology
    Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_1032">https://doi.org/10.15479/AT:ISTA:th_1032</a>'
  chicago: 'Case, Matthew J. “From the Left to the Right: A Tale of Asymmetries, Environments,
    and Hippocampal Development.” Institute of Science and Technology Austria, 2018.
    <a href="https://doi.org/10.15479/AT:ISTA:th_1032">https://doi.org/10.15479/AT:ISTA:th_1032</a>.'
  ieee: 'M. J. Case, “From the left to the right: A tale of asymmetries, environments,
    and hippocampal development,” Institute of Science and Technology Austria, 2018.'
  ista: 'Case MJ. 2018. From the left to the right: A tale of asymmetries, environments,
    and hippocampal development. Institute of Science and Technology Austria.'
  mla: 'Case, Matthew J. <i>From the Left to the Right: A Tale of Asymmetries, Environments,
    and Hippocampal Development</i>. Institute of Science and Technology Austria,
    2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_1032">10.15479/AT:ISTA:th_1032</a>.'
  short: 'M.J. Case, From the Left to the Right: A Tale of Asymmetries, Environments,
    and Hippocampal Development, Institute of Science and Technology Austria, 2018.'
corr_author: '1'
date_created: 2018-12-11T11:44:22Z
date_published: 2018-06-27T00:00:00Z
date_updated: 2026-07-31T09:40:17Z
day: '27'
ddc:
- '571'
- '576'
degree_awarded: PhD
department:
- _id: RySh
- _id: GradSch
doi: 10.15479/AT:ISTA:th_1032
doi_confirm: '1'
file:
- access_level: closed
  checksum: dcc7b55619d8509dd62b8e99d6cdee44
  content_type: application/msword
  creator: dernst
  date_created: 2019-04-09T07:16:26Z
  date_updated: 2021-02-11T23:30:13Z
  embargo_to: open_access
  file_id: '6251'
  file_name: 2018_Thesis_Case_Source.doc
  file_size: 141270528
  relation: source_file
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  checksum: f69fdd5c8709c4e618aa8c1a1221153d
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-09T07:16:23Z
  date_updated: 2021-02-11T11:17:14Z
  embargo: 2019-07-05
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  relation: main_file
file_date_updated: 2021-02-11T23:30:13Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th_1032
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '186'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8003'
pubrep_id: '1032'
related_material:
  record:
  - id: '682'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
title: 'From the left to the right: A tale of asymmetries, environments, and hippocampal
  development'
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
OA_place: publisher
_id: '10'
abstract:
- lang: eng
  text: Genomic imprinting is an epigenetic process that leads to parent of origin-specific
    gene expression in a subset of genes. Imprinted genes are essential for brain
    development, and deregulation of imprinting is associated with neurodevelopmental
    diseases and the pathogenesis of psychiatric disorders. However, the cell-type
    specificity of imprinting at single cell resolution, and how imprinting and thus
    gene dosage regulates neuronal circuit assembly is still largely unknown. Here,
    MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic
    imprinting at single cell level. By visualizing MADM-induced uniparental disomies
    (UPDs) in distinct colors at single cell level in genetic mosaic animals, this
    experimental paradigm provides a unique quantitative platform to systematically
    assay the UPD-mediated imbalances in imprinted gene expression at unprecedented
    resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics
    analysis was established and applied to systematically map cell-type-specific
    ‘imprintomes’ in the mouse brain. The results revealed that parental-specific
    expression of imprinted genes per se is rarely cell-type-specific even at the
    individual cell level. Conversely, when we extended the comparison to downstream
    responses resulting from imbalanced imprinted gene expression, we discovered an
    unexpectedly high degree of cell-type specificity. Furthermore, we determined
    a novel function of genomic imprinting in cortical astrocyte production and in
    olfactory bulb (OB) granule cell generation. These results suggest important functional
    implication of genomic imprinting for generating cell-type diversity in the brain.
    In addition, MADM provides a powerful tool to study candidate genes by concomitant
    genetic manipulation and fluorescent labelling of single cells. MADM-based candidate
    gene approach was utilized to identify potential imprinted genes involved in the
    generation of cortical astrocytes and OB granule cells. We investigated p57Kip2,
    a maternally expressed gene and known cell cycle regulator. Although we found
    that p57Kip2 does not play a role in these processes, we detected an unexpected
    function of the paternal allele previously thought to be silent. Finally, we took
    advantage of a key property of MADM which is to allow unambiguous investigation
    of environmental impact on single cells. The experimental pipeline based on FACS
    and RNA-seq analysis of MADM-labeled cells was established to probe the functional
    differences of single cell loss of gene function compared to global loss of function
    on a transcriptional level. With this method, both common and distinct responses
    were isolated due to cell-autonomous and non-autonomous effects acting on genotypically
    identical cells. As a result, transcriptional changes were identified which result
    solely from the surrounding environment. Using the MADM technology to study genomic
    imprinting at single cell resolution, we have identified cell-type-specific gene
    expression, novel gene function and the impact of environment on single cell transcriptomes.
    Together, these provide important insights to the understanding of mechanisms
    regulating cell-type specificity and thus diversity in the brain.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Susanne
  full_name: Laukoter, Susanne
  id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
  last_name: Laukoter
  orcid: 0000-0002-7903-3010
citation:
  ama: Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139.
    doi:<a href="https://doi.org/10.15479/AT:ISTA:th1057">10.15479/AT:ISTA:th1057</a>
  apa: Laukoter, S. (2018). <i>Role of genomic imprinting in cerebral cortex development</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th1057">https://doi.org/10.15479/AT:ISTA:th1057</a>
  chicago: Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.”
    Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th1057">https://doi.org/10.15479/AT:ISTA:th1057</a>.
  ieee: S. Laukoter, “Role of genomic imprinting in cerebral cortex development,”
    Institute of Science and Technology Austria, 2018.
  ista: Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development.
    Institute of Science and Technology Austria.
  mla: Laukoter, Susanne. <i>Role of Genomic Imprinting in Cerebral Cortex Development</i>.
    Institute of Science and Technology Austria, 2018, pp. 1–139, doi:<a href="https://doi.org/10.15479/AT:ISTA:th1057">10.15479/AT:ISTA:th1057</a>.
  short: S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute
    of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:08Z
date_published: 2018-11-21T00:00:00Z
date_updated: 2026-07-29T13:40:27Z
day: '21'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
- _id: GradSch
doi: 10.15479/AT:ISTA:th1057
doi_confirm: '1'
file:
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  date_updated: 2021-02-11T11:17:16Z
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file_date_updated: 2021-02-11T11:17:16Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th1057
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 1 - 139
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8046'
pubrep_id: '1057'
status: public
supervisor:
- first_name: Beatriz
  full_name: Vicoso, Beatriz
  id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
  last_name: Vicoso
  orcid: 0000-0002-4579-8306
title: Role of genomic imprinting in cerebral cortex development
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
OA_place: publisher
_id: '539'
abstract:
- lang: eng
  text: The whole life cycle of plants as well as their responses to environmental
    stimuli is governed by a complex network of hormonal regulations. A number of
    studies have demonstrated an essential role of both auxin and cytokinin in the
    regulation of many aspects of plant growth and development including embryogenesis,
    postembryonic organogenic processes such as root, and shoot branching, root and
    shoot apical meristem activity and phyllotaxis. Over the last decades essential
    knowledge on the key molecular factors and pathways that spatio-temporally define
    auxin and cytokinin activities in the plant body has accumulated. However, how
    both hormonal pathways are interconnected by a complex network of interactions
    and feedback circuits that determines the final outcome of the individual hormone
    actions is still largely unknown. Root system architecture establishment and in
    particular formation of lateral organs is prime example of developmental process
    at whose regulation both auxin and cytokinin pathways converge. To dissect convergence
    points and pathways that tightly balance auxin - cytokinin antagonistic activities
    that determine the root branching pattern transcriptome profiling was applied.
    Genome wide expression analyses of the xylem pole pericycle, a tissue giving rise
    to lateral roots, led to identification of genes that are highly responsive to
    combinatorial auxin and cytokinin treatments and play an essential function in
    the auxin-cytokinin regulated root branching. SYNERGISTIC AUXIN CYTOKININ 1 (SYAC1)
    gene, which encodes for a protein of unknown function, was detected among the
    top candidate genes of which expression was synergistically up-regulated by simultaneous
    hormonal treatment. Plants with modulated SYAC1 activity exhibit severe defects
    in the root system establishment and attenuate developmental responses to both
    auxin and cytokinin. To explore the biological function of the SYAC1, we employed
    different strategies including expression pattern analysis, subcellular localization
    and phenotypic analyses of the syac1 loss-of-function and gain-of-function transgenic
    lines along with the identification of the SYAC1 interaction partners. Detailed
    functional characterization revealed that SYAC1 acts as a developmentally specific
    regulator of the secretory pathway to control deposition of cell wall components
    and thereby rapidly fine tune elongation growth.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Andrej
  full_name: Hurny, Andrej
  id: 4DC4AF46-F248-11E8-B48F-1D18A9856A87
  last_name: Hurny
  orcid: 0000-0003-3638-1426
citation:
  ama: Hurny A. Identification and characterization of novel auxin-cytokinin cross-talk
    components. 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th_930">10.15479/AT:ISTA:th_930</a>
  apa: Hurny, A. (2018). <i>Identification and characterization of novel auxin-cytokinin
    cross-talk components</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_930">https://doi.org/10.15479/AT:ISTA:th_930</a>
  chicago: Hurny, Andrej. “Identification and Characterization of Novel Auxin-Cytokinin
    Cross-Talk Components.” Institute of Science and Technology Austria, 2018. <a
    href="https://doi.org/10.15479/AT:ISTA:th_930">https://doi.org/10.15479/AT:ISTA:th_930</a>.
  ieee: A. Hurny, “Identification and characterization of novel auxin-cytokinin cross-talk
    components,” Institute of Science and Technology Austria, 2018.
  ista: Hurny A. 2018. Identification and characterization of novel auxin-cytokinin
    cross-talk components. Institute of Science and Technology Austria.
  mla: Hurny, Andrej. <i>Identification and Characterization of Novel Auxin-Cytokinin
    Cross-Talk Components</i>. Institute of Science and Technology Austria, 2018,
    doi:<a href="https://doi.org/10.15479/AT:ISTA:th_930">10.15479/AT:ISTA:th_930</a>.
  short: A. Hurny, Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk
    Components, Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:47:03Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-07-29T13:30:01Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: EvBe
- _id: GradSch
doi: 10.15479/AT:ISTA:th_930
doi_confirm: '1'
file:
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  date_created: 2019-04-05T09:37:56Z
  date_updated: 2020-12-02T23:30:08Z
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  creator: dernst
  date_created: 2019-04-05T09:37:55Z
  date_updated: 2020-12-02T09:52:16Z
  embargo: 2019-07-10
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file_date_updated: 2020-12-02T23:30:08Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th_930
has_accepted_license: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: '147'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7277'
pubrep_id: '930'
related_material:
  record:
  - id: '1024'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Eva
  full_name: Benková, Eva
  id: 38F4F166-F248-11E8-B48F-1D18A9856A87
  last_name: Benková
  orcid: 0000-0002-8510-9739
title: Identification and characterization of novel auxin-cytokinin cross-talk components
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: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
_id: '544'
abstract:
- lang: eng
  text: Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes,
    are essential for immune responses, but also play key roles from early development
    to death through their interactions with other cell types. They regulate homeostasis
    and signaling during development, stem cell proliferation, metabolism, cancer,
    wound responses and aging, displaying intriguing molecular and functional conservation
    with vertebrate macrophages. Given the relative ease of genetics in Drosophila
    compared to vertebrates, tools permitting visualization and genetic manipulation
    of plasmatocytes and surrounding tissues independently at all stages would greatly
    aid in fully understanding these processes, but are lacking. Here we describe
    a comprehensive set of transgenic lines that allow this. These include extremely
    brightly fluorescing mCherry-based lines that allow GAL4-independent visualization
    of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8
    through adulthood in both live and fixed samples even as heterozygotes, greatly
    facilitating screening. These lines allow live visualization and tracking of embryonic
    plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing
    with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes
    and inner tissues can be seen in live or fixed embryos, larvae and adults. They
    permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout
    life. To facilitate genetic analysis of reciprocal signaling, we have also made
    a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers
    allows independent genetic manipulation of both plasmatocytes and surrounding
    tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes,
    both of which function from the early embryo to the adult.
acknowledged_ssus:
- _id: LifeSc
acknowledgement: ' A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko
  Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner
  by DOC Fellowships from the Austrian Academy of Sciences, '
article_processing_charge: No
author:
- first_name: Attila
  full_name: György, Attila
  id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
  last_name: György
  orcid: 0000-0002-1819-198X
- first_name: Marko
  full_name: Roblek, Marko
  id: 3047D808-F248-11E8-B48F-1D18A9856A87
  last_name: Roblek
  orcid: 0000-0001-9588-1389
- first_name: Aparna
  full_name: Ratheesh, Aparna
  id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
  last_name: Ratheesh
  orcid: 0000-0001-7190-0776
- first_name: Katarina
  full_name: Valosková, Katarina
  id: 46F146FC-F248-11E8-B48F-1D18A9856A87
  last_name: Valosková
  orcid: 0000-0002-7926-0221
- first_name: Vera
  full_name: Belyaeva, Vera
  id: 47F080FE-F248-11E8-B48F-1D18A9856A87
  last_name: Belyaeva
- first_name: Stephanie
  full_name: Wachner, Stephanie
  id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
  last_name: Wachner
- first_name: Yutaka
  full_name: Matsubayashi, Yutaka
  last_name: Matsubayashi
- first_name: Besaiz
  full_name: Sanchez Sanchez, Besaiz
  last_name: Sanchez Sanchez
- first_name: Brian
  full_name: Stramer, Brian
  last_name: Stramer
- first_name: Daria E
  full_name: Siekhaus, Daria E
  id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
  last_name: Siekhaus
  orcid: 0000-0001-8323-8353
citation:
  ama: 'György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization
    and genetic manipulation of Drosophila melanogaster macrophages and surrounding
    tissues. <i>G3: Genes, Genomes, Genetics</i>. 2018;8(3):845-857. doi:<a href="https://doi.org/10.1534/g3.117.300452">10.1534/g3.117.300452</a>'
  apa: 'György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner,
    S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic
    manipulation of Drosophila melanogaster macrophages and surrounding tissues. <i>G3:
    Genes, Genomes, Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/g3.117.300452">https://doi.org/10.1534/g3.117.300452</a>'
  chicago: 'György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera
    Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian
    Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic
    Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
    <i>G3: Genes, Genomes, Genetics</i>. Genetics Society of America, 2018. <a href="https://doi.org/10.1534/g3.117.300452">https://doi.org/10.1534/g3.117.300452</a>.'
  ieee: 'A. György <i>et al.</i>, “Tools allowing independent visualization and genetic
    manipulation of Drosophila melanogaster macrophages and surrounding tissues,”
    <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3. Genetics Society of America,
    pp. 845–857, 2018.'
  ista: 'György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi
    Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent
    visualization and genetic manipulation of Drosophila melanogaster macrophages
    and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.'
  mla: 'György, Attila, et al. “Tools Allowing Independent Visualization and Genetic
    Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
    <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3, Genetics Society of America,
    2018, pp. 845–57, doi:<a href="https://doi.org/10.1534/g3.117.300452">10.1534/g3.117.300452</a>.'
  short: 'A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner,
    Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes,
    Genetics 8 (2018) 845–857.'
corr_author: '1'
date_created: 2018-12-11T11:47:05Z
date_published: 2018-03-01T00:00:00Z
date_updated: 2026-10-06T22:31:08Z
day: '01'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1534/g3.117.300452
ec_funded: 1
external_id:
  isi:
  - '000426693300011'
file:
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  checksum: 7d9d28b915159078a4ca7add568010e8
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:11:48Z
  date_updated: 2020-07-14T12:46:56Z
  file_id: '4905'
  file_name: IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf
  file_size: 2251222
  relation: main_file
file_date_updated: 2020-07-14T12:46:56Z
fulldoi: https://doi.org/10.1534/g3.117.300452
has_accepted_license: '1'
intvolume: '         8'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 845 - 857
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2637E9C0-B435-11E9-9278-68D0E5697425
  grant_number: LSC16-021
  name: Investigating the role of the novel major superfamily facilitator transporter
    family member MFSD1 in metastasis
- _id: 2536F660-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '334077'
  name: Investigating the role of transporters in invasive migration through junctions
publication: 'G3: Genes, Genomes, Genetics'
publication_status: published
publisher: Genetics Society of America
publist_id: '7271'
pubrep_id: '990'
quality_controlled: '1'
related_material:
  record:
  - id: '6530'
    relation: research_paper
  - id: '6543'
    relation: research_paper
  - id: '11193'
    relation: dissertation_contains
    status: public
  - id: '6546'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Tools allowing independent visualization and genetic manipulation of Drosophila
  melanogaster macrophages and surrounding tissues
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2018'
...
---
OA_place: publisher
_id: '9'
abstract:
- lang: eng
  text: 'Immune cells migrating to the sites of infection navigate through diverse
    tissue architectures and switch their migratory mechanisms upon demand. However,
    little is known about systemic regulators that could allow the acquisition of
    these mechanisms. We performed a genetic screen in Drosophila melanogaster to
    identify regulators of germband invasion by embryonic macrophages into the confined
    space between the ectoderm and mesoderm. We have found that bZIP circadian transcription
    factors (TFs) Kayak (dFos) and Vrille (dNFIL3) have opposite effects on macrophage
    germband infiltration: Kayak facilitated and Vrille inhibited it. These TFs are
    enriched in the macrophages during migration and genetically interact to control
    it. Kayak sets a less coordinated mode of migration of the macrophage group and
    increases the probability and length of Levy walks. Intriguingly, the motility
    of kayak mutant macrophages was also strongly affected during initial germband
    invasion but not along another less confined route. Inhibiting Rho1 signaling
    within the tail ectoderm partially rescued the Kayak mutant phenotype, strongly
    suggesting that migrating macrophages have to overcome a barrier imposed by the
    stiffness of the ectoderm. Also, Kayak appeared to be important for the maintenance
    of the round cell shape and the rear edge translocation of the macrophages invading
    the germband. Complementary to this, the cortical actin cytoskeleton of Kayak-
    deficient macrophages was strongly affected. RNA sequencing revealed the filamin
    Cheerio and tetraspanin TM4SF to be downstream of Kayak. Chromatin immunoprecipitation
    and immunostaining revealed that the formin Diaphanous is another downstream target
    of Kayak. Immunostaining revealed that the formin Diaphanous is another downstream
    target of Kayak. Indeed, Cheerio, TM4SF and Diaphanous are required within macrophages
    for germband invasion, and expression of constitutively active Diaphanous in macrophages
    was able to rescue the kayak mutant phenotype. Moreover, Cher and Diaphanous are
    also reduced in the macrophages overexpressing Vrille. We hypothesize that Kayak,
    through its targets, increases actin polymerization and cortical tension in macrophages
    and thus allows extra force generation necessary for macrophage dissemination
    and migration through confined stiff tissues, while Vrille counterbalances it.'
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Vera
  full_name: Belyaeva, Vera
  id: 47F080FE-F248-11E8-B48F-1D18A9856A87
  last_name: Belyaeva
citation:
  ama: Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila
    melanogaster embryo . 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th1064">10.15479/AT:ISTA:th1064</a>
  apa: Belyaeva, V. (2018). <i>Transcriptional regulation of macrophage migration
    in the Drosophila melanogaster embryo </i>. Institute of Science and Technology
    Austria. <a href="https://doi.org/10.15479/AT:ISTA:th1064">https://doi.org/10.15479/AT:ISTA:th1064</a>
  chicago: Belyaeva, Vera. “Transcriptional Regulation of Macrophage Migration in
    the Drosophila Melanogaster Embryo .” Institute of Science and Technology Austria,
    2018. <a href="https://doi.org/10.15479/AT:ISTA:th1064">https://doi.org/10.15479/AT:ISTA:th1064</a>.
  ieee: V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila
    melanogaster embryo ,” Institute of Science and Technology Austria, 2018.
  ista: Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the
    Drosophila melanogaster embryo . Institute of Science and Technology Austria.
  mla: Belyaeva, Vera. <i>Transcriptional Regulation of Macrophage Migration in the
    Drosophila Melanogaster Embryo </i>. Institute of Science and Technology Austria,
    2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th1064">10.15479/AT:ISTA:th1064</a>.
  short: V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila
    Melanogaster Embryo , Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:08Z
date_published: 2018-07-01T00:00:00Z
date_updated: 2026-09-02T08:54:56Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: DaSi
- _id: GradSch
doi: 10.15479/AT:ISTA:th1064
doi_confirm: '1'
file:
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  checksum: d27b2465cb70d0c9678a0381b9b6ced1
  content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
  creator: dernst
  date_created: 2019-04-08T14:13:12Z
  date_updated: 2020-07-14T12:48:14Z
  embargo_to: open_access
  file_id: '6243'
  file_name: 2018_Thesis_Belyaeva_source.docx
  file_size: 102737483
  relation: source_file
- access_level: open_access
  checksum: a2939b61bde2de7b8ced77bbae0eaaed
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-08T14:14:08Z
  date_updated: 2021-02-11T11:17:16Z
  embargo: 2019-11-19
  file_id: '6244'
  file_name: 2018_Thesis_Belyaeva.pdf
  file_size: 88077843
  relation: main_file
file_date_updated: 2021-02-11T11:17:16Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th1064
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '96'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8047'
pubrep_id: '1064'
status: public
supervisor:
- first_name: Daria E
  full_name: Siekhaus, Daria E
  id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
  last_name: Siekhaus
  orcid: 0000-0001-8323-8353
title: 'Transcriptional regulation of macrophage migration in the Drosophila melanogaster
  embryo '
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
OA_place: publisher
_id: '6266'
abstract:
- lang: eng
  text: 'A major challenge in neuroscience research is to dissect the circuits that
    orchestrate behavior in health and disease. Proteins from a wide range of non-mammalian
    species, such as microbial opsins, have been successfully transplanted to specific
    neuronal targets to override their natural communication patterns. The goal of
    our work is to manipulate synaptic communication in a manner that closely incorporates
    the functional intricacies of synapses by preserving temporal encoding (i.e. the
    firing pattern of the presynaptic neuron) and connectivity (i.e. target specific
    synapses rather than specific neurons). Our strategy to achieve this goal builds
    on the use of non-mammalian transplants to create a synthetic synapse. The mode
    of modulation comes from pre-synaptic uptake of a synthetic neurotransmitter (SN)
    into synaptic vesicles by means of a genetically targeted transporter selective
    for the SN. Upon natural vesicular release, exposure of the SN to the synaptic
    cleft will modify the post-synaptic potential through an orthogonal ligand gated
    ion channel. To achieve this goal we have functionally characterized a mixed cationic
    methionine-gated ion channel from Arabidopsis thaliana, designed a method to functionally
    characterize a synthetic transporter in isolated synaptic vesicles without the
    need for transgenic animals, identified and extracted multiple prokaryotic uptake
    systems that are substrate specific for methionine (Met), and established a primary/cell
    line co-culture system that would allow future combinatorial testing of this orthogonal
    transmitter-transporter-channel trifecta. Synthetic synapses will provide a unique
    opportunity to manipulate synaptic communication while maintaining the electrophysiological
    integrity of the pre-synaptic cell. In this way, information may be preserved
    that was generated in upstream circuits and that could be essential for concerted
    function and information processing. '
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Catherine
  full_name: Mckenzie, Catherine
  id: 3EEDE19A-F248-11E8-B48F-1D18A9856A87
  last_name: Mckenzie
citation:
  ama: Mckenzie C. Design and characterization of methods and biological components
    to realize synthetic neurotransmission . 2018. doi:<a href="https://doi.org/10.15479/at:ista:th_1055">10.15479/at:ista:th_1055</a>
  apa: Mckenzie, C. (2018). <i>Design and characterization of methods and biological
    components to realize synthetic neurotransmission </i>. Institute of Science and
    Technology Austria. <a href="https://doi.org/10.15479/at:ista:th_1055">https://doi.org/10.15479/at:ista:th_1055</a>
  chicago: Mckenzie, Catherine. “Design and Characterization of Methods and Biological
    Components to Realize Synthetic Neurotransmission .” Institute of Science and
    Technology Austria, 2018. <a href="https://doi.org/10.15479/at:ista:th_1055">https://doi.org/10.15479/at:ista:th_1055</a>.
  ieee: C. Mckenzie, “Design and characterization of methods and biological components
    to realize synthetic neurotransmission ,” Institute of Science and Technology
    Austria, 2018.
  ista: Mckenzie C. 2018. Design and characterization of methods and biological components
    to realize synthetic neurotransmission . Institute of Science and Technology Austria.
  mla: Mckenzie, Catherine. <i>Design and Characterization of Methods and Biological
    Components to Realize Synthetic Neurotransmission </i>. Institute of Science and
    Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/at:ista:th_1055">10.15479/at:ista:th_1055</a>.
  short: C. Mckenzie, Design and Characterization of Methods and Biological Components
    to Realize Synthetic Neurotransmission , Institute of Science and Technology Austria,
    2018.
corr_author: '1'
date_created: 2019-04-09T14:13:39Z
date_published: 2018-10-31T00:00:00Z
date_updated: 2026-09-03T06:34:46Z
day: '31'
ddc:
- '571'
- '573'
degree_awarded: PhD
department:
- _id: HaJa
- _id: GradSch
doi: 10.15479/at:ista:th_1055
doi_confirm: '1'
file:
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  checksum: 9d2c2dca04b00e485470c28b262af59a
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-09T14:12:40Z
  date_updated: 2021-02-11T11:17:16Z
  embargo: 2019-11-24
  file_id: '6267'
  file_name: 2018_Thesis_McKenzie.pdf
  file_size: 4906420
  relation: main_file
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  creator: dernst
  date_created: 2019-04-09T14:12:40Z
  date_updated: 2020-07-14T12:47:25Z
  embargo_to: open_access
  file_id: '6268'
  file_name: 2018_Thesis_McKenzie_source.docx
  file_size: 5053545
  relation: source_file
file_date_updated: 2021-02-11T11:17:16Z
fulldoi: https://doi.org/10.15479/at:ista:th_1055
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '95'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
pubrep_id: '1055'
related_material:
  record:
  - id: '7132'
    relation: new_edition
    status: public
status: public
supervisor:
- first_name: Harald L
  full_name: Janovjak, Harald L
  id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
  last_name: Janovjak
  orcid: 0000-0002-8023-9315
title: 'Design and characterization of methods and biological components to realize
  synthetic neurotransmission '
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
_id: '5914'
abstract:
- lang: eng
  text: With the advent of optogenetics, it became possible to change the activity
    of a targeted population of neurons in a temporally controlled manner. To combine
    the advantages of 60-channel in vivo tetrode recording and laser-based optogenetics,
    we have developed a closed-loop recording system that allows for the actual electrophysiological
    signal to be used as a trigger for the laser light mediating the optogenetic intervention.
    We have optimized the weight, size, and shape of the corresponding implant to
    make it compatible with the size, force, and movements of a behaving mouse, and
    we have shown that the system can efficiently block sharp wave ripple (SWR) events
    using those events themselves as a trigger. To demonstrate the full potential
    of the optogenetic recording system we present a pilot study addressing the contribution
    of SWR events to learning in a complex behavioral task.
article_number: e0087
article_processing_charge: No
author:
- first_name: Dámaris K
  full_name: Rangel Guerrero, Dámaris K
  id: 4871BCE6-F248-11E8-B48F-1D18A9856A87
  last_name: Rangel Guerrero
  orcid: 0000-0002-8602-4374
- first_name: James G.
  full_name: Donnett, James G.
  last_name: Donnett
- first_name: Jozsef L
  full_name: Csicsvari, Jozsef L
  id: 3FA14672-F248-11E8-B48F-1D18A9856A87
  last_name: Csicsvari
  orcid: 0000-0002-5193-4036
- first_name: Krisztián
  full_name: Kovács, Krisztián
  id: 2AB5821E-F248-11E8-B48F-1D18A9856A87
  last_name: Kovács
  orcid: 0000-0001-6251-1007
citation:
  ama: 'Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. Tetrode recording
    from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop
    optogenetics: A technique to study the contribution of Hippocampal SWR events
    to learning. <i>eNeuro</i>. 2018;5(4). doi:<a href="https://doi.org/10.1523/ENEURO.0087-18.2018">10.1523/ENEURO.0087-18.2018</a>'
  apa: 'Rangel Guerrero, D. K., Donnett, J. G., Csicsvari, J. L., &#38; Kovács, K.
    (2018). Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation
    closed-loop optogenetics: A technique to study the contribution of Hippocampal
    SWR events to learning. <i>ENeuro</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/ENEURO.0087-18.2018">https://doi.org/10.1523/ENEURO.0087-18.2018</a>'
  chicago: 'Rangel Guerrero, Dámaris K, James G. Donnett, Jozsef L Csicsvari, and
    Krisztián Kovács. “Tetrode Recording from the Hippocampus of Behaving Mice Coupled
    with Four-Point-Irradiation Closed-Loop Optogenetics: A Technique to Study the
    Contribution of Hippocampal SWR Events to Learning.” <i>ENeuro</i>. Society for
    Neuroscience, 2018. <a href="https://doi.org/10.1523/ENEURO.0087-18.2018">https://doi.org/10.1523/ENEURO.0087-18.2018</a>.'
  ieee: 'D. K. Rangel Guerrero, J. G. Donnett, J. L. Csicsvari, and K. Kovács, “Tetrode
    recording from the hippocampus of behaving mice coupled with four-point-irradiation
    closed-loop optogenetics: A technique to study the contribution of Hippocampal
    SWR events to learning,” <i>eNeuro</i>, vol. 5, no. 4. Society for Neuroscience,
    2018.'
  ista: 'Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. 2018. Tetrode recording
    from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop
    optogenetics: A technique to study the contribution of Hippocampal SWR events
    to learning. eNeuro. 5(4), e0087.'
  mla: 'Rangel Guerrero, Dámaris K., et al. “Tetrode Recording from the Hippocampus
    of Behaving Mice Coupled with Four-Point-Irradiation Closed-Loop Optogenetics:
    A Technique to Study the Contribution of Hippocampal SWR Events to Learning.”
    <i>ENeuro</i>, vol. 5, no. 4, e0087, Society for Neuroscience, 2018, doi:<a href="https://doi.org/10.1523/ENEURO.0087-18.2018">10.1523/ENEURO.0087-18.2018</a>.'
  short: D.K. Rangel Guerrero, J.G. Donnett, J.L. Csicsvari, K. Kovács, ENeuro 5 (2018).
date_created: 2019-02-03T22:59:16Z
date_published: 2018-07-27T00:00:00Z
date_updated: 2026-10-06T22:31:09Z
day: '27'
ddc:
- '570'
department:
- _id: JoCs
doi: 10.1523/ENEURO.0087-18.2018
ec_funded: 1
external_id:
  isi:
  - '000443994700007'
file:
- access_level: open_access
  checksum: f4915d45fc7ad4648b7b7a13fdecca01
  content_type: application/pdf
  creator: dernst
  date_created: 2019-02-05T12:48:36Z
  date_updated: 2020-07-14T12:47:13Z
  file_id: '5921'
  file_name: 2018_ENeuro_Guerrero.pdf
  file_size: 3746884
  relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
fulldoi: https://doi.org/10.1523/ENEURO.0087-18.2018
has_accepted_license: '1'
intvolume: '         5'
isi: 1
issue: '4'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 257D4372-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I2072-B27
  name: Interneuron plasticity during spatial learning
publication: eNeuro
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
related_material:
  record:
  - id: '6849'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: 'Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation
  closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR
  events to learning'
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: 5
year: '2018'
...
---
_id: '542'
abstract:
- lang: eng
  text: The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a
    model for autosomal segregation distortion for close to a century, but several
    questions remain regarding its biology and evolutionary history. A recently published
    set of population genomics resources for wild mice includes several individuals
    heterozygous for the t-haplotype, which we use to characterize this selfish element
    at the genomic and transcriptomic level. Our results show that large sections
    of the t-haplotype have been replaced by standard homologous sequences, possibly
    due to occasional events of recombination, and that this complicates the inference
    of its history. As expected for a long genomic segment of very low recombination,
    the t-haplotype carries an excess of fixed nonsynonymous mutations compared to
    the standard chromosome. This excess is stronger for regions that have not undergone
    recent recombination, suggesting that occasional gene flow between the t and the
    standard chromosome may provide a mechanism to regenerate coding sequences that
    have accumulated deleterious mutations. Finally, we find that t-complex genes
    with altered expression largely overlap with deleted or amplified regions, and
    that carrying a t-haplotype alters the testis expression of genes outside of the
    t-complex, providing new leads into the pathways involved in the biology of this
    segregation distorter.
article_processing_charge: No
article_type: original
author:
- first_name: Réka K
  full_name: Kelemen, Réka K
  id: 48D3F8DE-F248-11E8-B48F-1D18A9856A87
  last_name: Kelemen
  orcid: 0000-0002-8489-9281
- first_name: Beatriz
  full_name: Vicoso, Beatriz
  id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
  last_name: Vicoso
  orcid: 0000-0002-4579-8306
citation:
  ama: Kelemen RK, Vicoso B. Complex history and differentiation patterns of the t-haplotype,
    a mouse meiotic driver. <i>Genetics</i>. 2018;208(1):365-375. doi:<a href="https://doi.org/10.1534/genetics.117.300513">10.1534/genetics.117.300513</a>
  apa: Kelemen, R. K., &#38; Vicoso, B. (2018). Complex history and differentiation
    patterns of the t-haplotype, a mouse meiotic driver. <i>Genetics</i>. Genetics
    Society of America. <a href="https://doi.org/10.1534/genetics.117.300513">https://doi.org/10.1534/genetics.117.300513</a>
  chicago: Kelemen, Réka K, and Beatriz Vicoso. “Complex History and Differentiation
    Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>. Genetics
    Society of America, 2018. <a href="https://doi.org/10.1534/genetics.117.300513">https://doi.org/10.1534/genetics.117.300513</a>.
  ieee: R. K. Kelemen and B. Vicoso, “Complex history and differentiation patterns
    of the t-haplotype, a mouse meiotic driver,” <i>Genetics</i>, vol. 208, no. 1.
    Genetics Society of America, pp. 365–375, 2018.
  ista: Kelemen RK, Vicoso B. 2018. Complex history and differentiation patterns of
    the t-haplotype, a mouse meiotic driver. Genetics. 208(1), 365–375.
  mla: Kelemen, Réka K., and Beatriz Vicoso. “Complex History and Differentiation
    Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>, vol. 208,
    no. 1, Genetics Society of America, 2018, pp. 365–75, doi:<a href="https://doi.org/10.1534/genetics.117.300513">10.1534/genetics.117.300513</a>.
  short: R.K. Kelemen, B. Vicoso, Genetics 208 (2018) 365–375.
corr_author: '1'
date_created: 2018-12-11T11:47:04Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-10-06T22:31:17Z
day: '01'
ddc:
- '576'
department:
- _id: BeVi
doi: 10.1534/genetics.117.300513
ec_funded: 1
external_id:
  isi:
  - '000419356300024'
file:
- access_level: open_access
  checksum: 2123845e7031a0cf043905be160f9e69
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:14Z
  date_updated: 2020-07-14T12:46:50Z
  file_id: '5132'
  file_name: IST-2018-1058-v1+1_365.full__1_.pdf
  file_size: 1311661
  relation: main_file
file_date_updated: 2020-07-14T12:46:50Z
fulldoi: https://doi.org/10.1534/genetics.117.300513
has_accepted_license: '1'
intvolume: '       208'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 365 - 375
project:
- _id: 250BDE62-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715257'
  name: Prevalence and Influence of Sexual Antagonism on Genome Evolution
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '7274'
pubrep_id: '1058'
quality_controlled: '1'
related_material:
  record:
  - id: '5571'
    relation: popular_science
    status: public
  - id: '5572'
    relation: popular_science
    status: public
  - id: '17119'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Complex history and differentiation patterns of the t-haplotype, a mouse meiotic
  driver
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 208
year: '2018'
...
---
_id: '1084'
abstract:
- lang: eng
  text: 'BceRS and PsdRS are paralogous two-component systems in Bacillus subtilis
    controlling the response to antimicrobial peptides. In the presence of extracellular
    bacitracin and nisin, respectively, the two response regulators (RRs) bind their
    target promoters, PbceA or PpsdA, resulting in a strong up-regulation of target
    gene expression and ultimately antibiotic resistance. Despite high sequence similarity
    between the RRs BceR and PsdR and their known binding sites, no cross-regulation
    has been observed between them. We therefore investigated the specificity determinants
    of PbceA and PpsdA that ensure the insulation of these two paralogous pathways
    at the RR–promoter interface. In vivo and in vitro analyses demonstrate that the
    regulatory regions within these two promoters contain three important elements:
    in addition to the known (main) binding site, we identified a linker region and
    a secondary binding site that are crucial for functionality. Initial binding to
    the high-affinity, low-specificity main binding site is a prerequisite for the
    subsequent highly specific binding of a second RR dimer to the low-affinity secondary
    binding site. In addition to this hierarchical cooperative binding, discrimination
    requires a competition of the two RRs for their respective binding site mediated
    by only slight differences in binding affinities.'
article_processing_charge: No
author:
- first_name: Chong
  full_name: Fang, Chong
  last_name: Fang
- 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: Martin
  full_name: Grafe, Martin
  last_name: Grafe
- first_name: Ralf
  full_name: Heermann, Ralf
  last_name: Heermann
- first_name: Kirsten
  full_name: Jung, Kirsten
  last_name: Jung
- first_name: Susanne
  full_name: Gebhard, Susanne
  last_name: Gebhard
- first_name: Thorsten
  full_name: Mascher, Thorsten
  last_name: Mascher
citation:
  ama: Fang C, Nagy-Staron AA, Grafe M, et al. Insulation and wiring specificity of
    BceR like response regulators and their target promoters in Bacillus subtilis.
    <i>Molecular Microbiology</i>. 2017;104(1):16-31. doi:<a href="https://doi.org/10.1111/mmi.13597">10.1111/mmi.13597</a>
  apa: Fang, C., Nagy-Staron, A. A., Grafe, M., Heermann, R., Jung, K., Gebhard, S.,
    &#38; Mascher, T. (2017). Insulation and wiring specificity of BceR like response
    regulators and their target promoters in Bacillus subtilis. <i>Molecular Microbiology</i>.
    Wiley-Blackwell. <a href="https://doi.org/10.1111/mmi.13597">https://doi.org/10.1111/mmi.13597</a>
  chicago: Fang, Chong, Anna A Nagy-Staron, Martin Grafe, Ralf Heermann, Kirsten Jung,
    Susanne Gebhard, and Thorsten Mascher. “Insulation and Wiring Specificity of BceR
    like Response Regulators and Their Target Promoters in Bacillus Subtilis.” <i>Molecular
    Microbiology</i>. Wiley-Blackwell, 2017. <a href="https://doi.org/10.1111/mmi.13597">https://doi.org/10.1111/mmi.13597</a>.
  ieee: C. Fang <i>et al.</i>, “Insulation and wiring specificity of BceR like response
    regulators and their target promoters in Bacillus subtilis,” <i>Molecular Microbiology</i>,
    vol. 104, no. 1. Wiley-Blackwell, pp. 16–31, 2017.
  ista: Fang C, Nagy-Staron AA, Grafe M, Heermann R, Jung K, Gebhard S, Mascher T.
    2017. Insulation and wiring specificity of BceR like response regulators and their
    target promoters in Bacillus subtilis. Molecular Microbiology. 104(1), 16–31.
  mla: Fang, Chong, et al. “Insulation and Wiring Specificity of BceR like Response
    Regulators and Their Target Promoters in Bacillus Subtilis.” <i>Molecular Microbiology</i>,
    vol. 104, no. 1, Wiley-Blackwell, 2017, pp. 16–31, doi:<a href="https://doi.org/10.1111/mmi.13597">10.1111/mmi.13597</a>.
  short: C. Fang, A.A. Nagy-Staron, M. Grafe, R. Heermann, K. Jung, S. Gebhard, T.
    Mascher, Molecular Microbiology 104 (2017) 16–31.
date_created: 2018-12-11T11:50:03Z
date_published: 2017-04-01T00:00:00Z
date_updated: 2026-04-16T09:56:09Z
day: '01'
department:
- _id: CaGu
doi: 10.1111/mmi.13597
external_id:
  isi:
  - '000398059200002'
fulldoi: https://doi.org/10.1111/mmi.13597
intvolume: '       104'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa_version: None
page: 16 - 31
publication: Molecular Microbiology
publication_identifier:
  issn:
  - ' 0950-382X'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6294'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Insulation and wiring specificity of BceR like response regulators and their
  target promoters in Bacillus subtilis
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 104
year: '2017'
...
---
_id: '1085'
abstract:
- lang: eng
  text: Sex chromosomes evolve once recombination is halted between a homologous pair
    of chromosomes. The dominant model of sex chromosome evolution posits that recombination
    is suppressed between emerging X and Y chromosomes in order to resolve sexual
    conflict. Here we test this model using whole genome and transcriptome resequencing
    data in the guppy, a model for sexual selection with many Y-linked colour traits.
    We show that although the nascent Y chromosome encompasses nearly half of the
    linkage group, there has been no perceptible degradation of Y chromosome gene
    content or activity. Using replicate wild populations with differing levels of
    sexually antagonistic selection for colour, we also show that sexual selection
    leads to greater expansion of the non-recombining region and increased Y chromosome
    divergence. These results provide empirical support for longstanding models of
    sex chromosome catalysis, and suggest an important role for sexual selection and
    sexual conflict in genome evolution.
article_number: '14251'
article_processing_charge: No
author:
- first_name: Alison
  full_name: Wright, Alison
  last_name: Wright
- first_name: Iulia
  full_name: Darolti, Iulia
  last_name: Darolti
- first_name: Natasha
  full_name: Bloch, Natasha
  last_name: Bloch
- first_name: Vicencio
  full_name: Oostra, Vicencio
  last_name: Oostra
- first_name: Benjamin
  full_name: Sandkam, Benjamin
  last_name: Sandkam
- first_name: Séverine
  full_name: Buechel, Séverine
  last_name: Buechel
- first_name: Niclas
  full_name: Kolm, Niclas
  last_name: Kolm
- first_name: Felix
  full_name: Breden, Felix
  last_name: Breden
- first_name: Beatriz
  full_name: Vicoso, Beatriz
  id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
  last_name: Vicoso
  orcid: 0000-0002-4579-8306
- first_name: Judith
  full_name: Mank, Judith
  last_name: Mank
citation:
  ama: Wright A, Darolti I, Bloch N, et al. Convergent recombination suppression suggests
    role of sexual selection in guppy sex chromosome formation. <i>Nature Communications</i>.
    2017;8. doi:<a href="https://doi.org/10.1038/ncomms14251">10.1038/ncomms14251</a>
  apa: Wright, A., Darolti, I., Bloch, N., Oostra, V., Sandkam, B., Buechel, S., …
    Mank, J. (2017). Convergent recombination suppression suggests role of sexual
    selection in guppy sex chromosome formation. <i>Nature Communications</i>. Nature
    Publishing Group. <a href="https://doi.org/10.1038/ncomms14251">https://doi.org/10.1038/ncomms14251</a>
  chicago: Wright, Alison, Iulia Darolti, Natasha Bloch, Vicencio Oostra, Benjamin
    Sandkam, Séverine Buechel, Niclas Kolm, Felix Breden, Beatriz Vicoso, and Judith
    Mank. “Convergent Recombination Suppression Suggests Role of Sexual Selection
    in Guppy Sex Chromosome Formation.” <i>Nature Communications</i>. Nature Publishing
    Group, 2017. <a href="https://doi.org/10.1038/ncomms14251">https://doi.org/10.1038/ncomms14251</a>.
  ieee: A. Wright <i>et al.</i>, “Convergent recombination suppression suggests role
    of sexual selection in guppy sex chromosome formation,” <i>Nature Communications</i>,
    vol. 8. Nature Publishing Group, 2017.
  ista: Wright A, Darolti I, Bloch N, Oostra V, Sandkam B, Buechel S, Kolm N, Breden
    F, Vicoso B, Mank J. 2017. Convergent recombination suppression suggests role
    of sexual selection in guppy sex chromosome formation. Nature Communications.
    8, 14251.
  mla: Wright, Alison, et al. “Convergent Recombination Suppression Suggests Role
    of Sexual Selection in Guppy Sex Chromosome Formation.” <i>Nature Communications</i>,
    vol. 8, 14251, Nature Publishing Group, 2017, doi:<a href="https://doi.org/10.1038/ncomms14251">10.1038/ncomms14251</a>.
  short: A. Wright, I. Darolti, N. Bloch, V. Oostra, B. Sandkam, S. Buechel, N. Kolm,
    F. Breden, B. Vicoso, J. Mank, Nature Communications 8 (2017).
date_created: 2018-12-11T11:50:04Z
date_published: 2017-01-31T00:00:00Z
date_updated: 2025-07-10T11:50:01Z
day: '31'
ddc:
- '570'
- '576'
department:
- _id: BeVi
doi: 10.1038/ncomms14251
external_id:
  isi:
  - '000392953700001'
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:22Z
  date_updated: 2018-12-12T10:15:22Z
  file_id: '5141'
  file_name: IST-2017-791-v1+1_ncomms14251.pdf
  file_size: 955256
  relation: main_file
file_date_updated: 2018-12-12T10:15:22Z
fulldoi: https://doi.org/10.1038/ncomms14251
has_accepted_license: '1'
intvolume: '         8'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Nature Publishing Group
publist_id: '6292'
pubrep_id: '791'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Convergent recombination suppression suggests role of sexual selection in guppy
  sex chromosome formation
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: 8
year: '2017'
...
---
_id: '1086'
abstract:
- lang: eng
  text: 'Characterisation of G protein-coupled receptors (GPCR) relies on the availability
    of a toolbox of ligands that selectively modulate different functional states
    of the receptors. To uncover such molecules, we explored a unique strategy for
    ligand discovery that takes advantage of the evolutionary conservation of the
    600-million-year-old oxytocin/vasopressin signalling system. We isolated the insect
    oxytocin/vasopressin orthologue inotocin from the black garden ant (Lasius niger),
    identified and cloned its cognate receptor and determined its pharmacological
    properties on the insect and human oxytocin/vasopressin receptors. Subsequently,
    we identified a functional dichotomy: inotocin activated the insect inotocin and
    the human vasopressin V1b receptors, but inhibited the human V1aR. Replacement
    of Arg8 of inotocin by D-Arg8 led to a potent, stable and competitive V1aR-antagonist
    ([D-Arg8]-inotocin) with a 3,000-fold binding selectivity for the human V1aR over
    the other three subtypes, OTR, V1bR and V2R. The Arg8/D-Arg8 ligand-pair was further
    investigated to gain novel insights into the oxytocin/vasopressin peptide-receptor
    interaction, which led to the identification of key residues of the receptors
    that are important for ligand functionality and selectivity. These observations
    could play an important role for development of oxytocin/vasopressin receptor
    modulators that would enable clear distinction of the physiological and pathological
    responses of the individual receptor subtypes.'
article_processing_charge: No
author:
- first_name: Maria
  full_name: Di Giglio, Maria
  last_name: Di Giglio
- first_name: Markus
  full_name: Muttenthaler, Markus
  last_name: Muttenthaler
- first_name: Kasper
  full_name: Harpsøe, Kasper
  last_name: Harpsøe
- first_name: Zita
  full_name: Liutkeviciute, Zita
  last_name: Liutkeviciute
- first_name: Peter
  full_name: Keov, Peter
  last_name: Keov
- first_name: Thomas
  full_name: Eder, Thomas
  last_name: Eder
- first_name: Thomas
  full_name: Rattei, Thomas
  last_name: Rattei
- first_name: Sarah
  full_name: Arrowsmith, Sarah
  last_name: Arrowsmith
- first_name: Susan
  full_name: Wray, Susan
  last_name: Wray
- first_name: Ales
  full_name: Marek, Ales
  last_name: Marek
- first_name: Tomas
  full_name: Elbert, Tomas
  last_name: Elbert
- first_name: Paul
  full_name: Alewood, Paul
  last_name: Alewood
- first_name: David
  full_name: Gloriam, David
  last_name: Gloriam
- first_name: Christian
  full_name: Gruber, Christian
  last_name: Gruber
citation:
  ama: Di Giglio M, Muttenthaler M, Harpsøe K, et al. Development of a human vasopressin
    V1a-receptor antagonist from an evolutionary-related insect neuropeptide. <i>Scientific
    Reports</i>. 2017;7:41002. doi:<a href="https://doi.org/10.1038/srep41002">10.1038/srep41002</a>
  apa: Di Giglio, M., Muttenthaler, M., Harpsøe, K., Liutkeviciute, Z., Keov, P.,
    Eder, T., … Gruber, C. (2017). Development of a human vasopressin V1a-receptor
    antagonist from an evolutionary-related insect neuropeptide. <i>Scientific Reports</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/srep41002">https://doi.org/10.1038/srep41002</a>
  chicago: Di Giglio, Maria, Markus Muttenthaler, Kasper Harpsøe, Zita Liutkeviciute,
    Peter Keov, Thomas Eder, Thomas Rattei, et al. “Development of a Human Vasopressin
    V1a-Receptor Antagonist from an Evolutionary-Related Insect Neuropeptide.” <i>Scientific
    Reports</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/srep41002">https://doi.org/10.1038/srep41002</a>.
  ieee: M. Di Giglio <i>et al.</i>, “Development of a human vasopressin V1a-receptor
    antagonist from an evolutionary-related insect neuropeptide,” <i>Scientific Reports</i>,
    vol. 7. Nature Publishing Group, p. 41002, 2017.
  ista: Di Giglio M, Muttenthaler M, Harpsøe K, Liutkeviciute Z, Keov P, Eder T, Rattei
    T, Arrowsmith S, Wray S, Marek A, Elbert T, Alewood P, Gloriam D, Gruber C. 2017.
    Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related
    insect neuropeptide. Scientific Reports. 7, 41002.
  mla: Di Giglio, Maria, et al. “Development of a Human Vasopressin V1a-Receptor Antagonist
    from an Evolutionary-Related Insect Neuropeptide.” <i>Scientific Reports</i>,
    vol. 7, Nature Publishing Group, 2017, p. 41002, doi:<a href="https://doi.org/10.1038/srep41002">10.1038/srep41002</a>.
  short: M. Di Giglio, M. Muttenthaler, K. Harpsøe, Z. Liutkeviciute, P. Keov, T.
    Eder, T. Rattei, S. Arrowsmith, S. Wray, A. Marek, T. Elbert, P. Alewood, D. Gloriam,
    C. Gruber, Scientific Reports 7 (2017) 41002.
date_created: 2018-12-11T11:50:04Z
date_published: 2017-02-01T00:00:00Z
date_updated: 2023-09-20T11:47:47Z
day: '01'
ddc:
- '570'
- '590'
doi: 10.1038/srep41002
external_id:
  isi:
  - '000393163800001'
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:14:59Z
  date_updated: 2018-12-12T10:14:59Z
  file_id: '5115'
  file_name: IST-2017-790-v1+1_srep41002_1_.pdf
  file_size: 1994139
  relation: main_file
file_date_updated: 2018-12-12T10:14:59Z
fulldoi: https://doi.org/10.1038/srep41002
has_accepted_license: '1'
intvolume: '         7'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: '41002'
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '6291'
pubrep_id: '790'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related
  insect neuropeptide
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 7
year: '2017'
...
---
_id: '1087'
abstract:
- lang: eng
  text: Using extensive direct numerical simulations, the dynamics of laminar-turbulent
    fronts in pipe flow is investigated for Reynolds numbers between and 5500. We
    here investigate the physical distinction between the fronts of weak and strong
    slugs both by analysing the turbulent kinetic energy budget and by comparing the
    downstream front motion to the advection speed of bulk turbulent structures. Our
    study shows that weak downstream fronts travel slower than turbulent structures
    in the bulk and correspond to decaying turbulence at the front. At the downstream
    front speed becomes faster than the advection speed, marking the onset of strong
    fronts. In contrast to weak fronts, turbulent eddies are generated at strong fronts
    by feeding on the downstream laminar flow. Our study also suggests that temporal
    fluctuations of production and dissipation at the downstream laminar-turbulent
    front drive the dynamical switches between the two types of front observed up
    to.
acknowledged_ssus:
- _id: ScienComp
article_processing_charge: No
arxiv: 1
author:
- first_name: Baofang
  full_name: Song, Baofang
  last_name: Song
- first_name: Dwight
  full_name: Barkley, Dwight
  last_name: Barkley
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Marc
  full_name: Avila, Marc
  last_name: Avila
citation:
  ama: Song B, Barkley D, Hof B, Avila M. Speed and structure of turbulent fronts
    in pipe flow. <i>Journal of Fluid Mechanics</i>. 2017;813:1045-1059. doi:<a href="https://doi.org/10.1017/jfm.2017.14">10.1017/jfm.2017.14</a>
  apa: Song, B., Barkley, D., Hof, B., &#38; Avila, M. (2017). Speed and structure
    of turbulent fronts in pipe flow. <i>Journal of Fluid Mechanics</i>. Cambridge
    University Press. <a href="https://doi.org/10.1017/jfm.2017.14">https://doi.org/10.1017/jfm.2017.14</a>
  chicago: Song, Baofang, Dwight Barkley, Björn Hof, and Marc Avila. “Speed and Structure
    of Turbulent Fronts in Pipe Flow.” <i>Journal of Fluid Mechanics</i>. Cambridge
    University Press, 2017. <a href="https://doi.org/10.1017/jfm.2017.14">https://doi.org/10.1017/jfm.2017.14</a>.
  ieee: B. Song, D. Barkley, B. Hof, and M. Avila, “Speed and structure of turbulent
    fronts in pipe flow,” <i>Journal of Fluid Mechanics</i>, vol. 813. Cambridge University
    Press, pp. 1045–1059, 2017.
  ista: Song B, Barkley D, Hof B, Avila M. 2017. Speed and structure of turbulent
    fronts in pipe flow. Journal of Fluid Mechanics. 813, 1045–1059.
  mla: Song, Baofang, et al. “Speed and Structure of Turbulent Fronts in Pipe Flow.”
    <i>Journal of Fluid Mechanics</i>, vol. 813, Cambridge University Press, 2017,
    pp. 1045–59, doi:<a href="https://doi.org/10.1017/jfm.2017.14">10.1017/jfm.2017.14</a>.
  short: B. Song, D. Barkley, B. Hof, M. Avila, Journal of Fluid Mechanics 813 (2017)
    1045–1059.
date_created: 2018-12-11T11:50:04Z
date_published: 2017-02-25T00:00:00Z
date_updated: 2025-06-04T08:35:11Z
day: '25'
department:
- _id: BjHo
doi: 10.1017/jfm.2017.14
ec_funded: 1
external_id:
  arxiv:
  - '1603.04077'
  isi:
  - '000394376400044'
fulldoi: https://doi.org/10.1017/jfm.2017.14
intvolume: '       813'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1603.04077
month: '02'
oa: 1
oa_version: Submitted Version
page: 1045 - 1059
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
publication: Journal of Fluid Mechanics
publication_identifier:
  issn:
  - 0022-1120
publication_status: published
publisher: Cambridge University Press
publist_id: '6290'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Speed and structure of turbulent fronts in pipe flow
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 813
year: '2017'
...
---
_id: '1089'
abstract:
- lang: eng
  text: We discuss properties of distributions that are multivariate totally positive
    of order two (MTP2) related to conditional independence. In particular, we show
    that any independence model generated by an MTP2 distribution is a compositional
    semigraphoid which is upward-stable and singleton-transitive. In addition, we
    prove that any MTP2 distribution satisfying an appropriate support condition is
    faithful to its concentration graph. Finally, we analyze factorization properties
    of MTP2 distributions and discuss ways of constructing MTP2 distributions; in
    particular we give conditions on the log-linear parameters of a discrete distribution
    which ensure MTP2 and characterize conditional Gaussian distributions which satisfy
    MTP2.
article_processing_charge: No
arxiv: 1
author:
- first_name: Shaun
  full_name: Fallat, Shaun
  last_name: Fallat
- first_name: Steffen
  full_name: Lauritzen, Steffen
  last_name: Lauritzen
- first_name: Kayvan
  full_name: Sadeghi, Kayvan
  last_name: Sadeghi
- first_name: Caroline
  full_name: Uhler, Caroline
  id: 49ADD78E-F248-11E8-B48F-1D18A9856A87
  last_name: Uhler
  orcid: 0000-0002-7008-0216
- first_name: Nanny
  full_name: Wermuth, Nanny
  last_name: Wermuth
- first_name: Piotr
  full_name: Zwiernik, Piotr
  last_name: Zwiernik
citation:
  ama: Fallat S, Lauritzen S, Sadeghi K, Uhler C, Wermuth N, Zwiernik P. Total positivity
    in Markov structures. <i>Annals of Statistics</i>. 2017;45(3):1152-1184. doi:<a
    href="https://doi.org/10.1214/16-AOS1478">10.1214/16-AOS1478</a>
  apa: Fallat, S., Lauritzen, S., Sadeghi, K., Uhler, C., Wermuth, N., &#38; Zwiernik,
    P. (2017). Total positivity in Markov structures. <i>Annals of Statistics</i>.
    Institute of Mathematical Statistics. <a href="https://doi.org/10.1214/16-AOS1478">https://doi.org/10.1214/16-AOS1478</a>
  chicago: Fallat, Shaun, Steffen Lauritzen, Kayvan Sadeghi, Caroline Uhler, Nanny
    Wermuth, and Piotr Zwiernik. “Total Positivity in Markov Structures.” <i>Annals
    of Statistics</i>. Institute of Mathematical Statistics, 2017. <a href="https://doi.org/10.1214/16-AOS1478">https://doi.org/10.1214/16-AOS1478</a>.
  ieee: S. Fallat, S. Lauritzen, K. Sadeghi, C. Uhler, N. Wermuth, and P. Zwiernik,
    “Total positivity in Markov structures,” <i>Annals of Statistics</i>, vol. 45,
    no. 3. Institute of Mathematical Statistics, pp. 1152–1184, 2017.
  ista: Fallat S, Lauritzen S, Sadeghi K, Uhler C, Wermuth N, Zwiernik P. 2017. Total
    positivity in Markov structures. Annals of Statistics. 45(3), 1152–1184.
  mla: Fallat, Shaun, et al. “Total Positivity in Markov Structures.” <i>Annals of
    Statistics</i>, vol. 45, no. 3, Institute of Mathematical Statistics, 2017, pp.
    1152–84, doi:<a href="https://doi.org/10.1214/16-AOS1478">10.1214/16-AOS1478</a>.
  short: S. Fallat, S. Lauritzen, K. Sadeghi, C. Uhler, N. Wermuth, P. Zwiernik, Annals
    of Statistics 45 (2017) 1152–1184.
corr_author: '1'
date_created: 2018-12-11T11:50:05Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2025-06-04T08:35:37Z
day: '01'
department:
- _id: CaUh
doi: 10.1214/16-AOS1478
external_id:
  arxiv:
  - '1510.01290'
  isi:
  - '000404395900008'
fulldoi: https://doi.org/10.1214/16-AOS1478
intvolume: '        45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1510.01290
month: '06'
oa: 1
oa_version: Submitted Version
page: 1152 - 1184
project:
- _id: 2530CA10-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Y 903-N35
  name: 'Gaussian Graphical Models: Theory and Applications'
publication: Annals of Statistics
publication_identifier:
  issn:
  - 0090-5364
publication_status: published
publisher: Institute of Mathematical Statistics
publist_id: '6288'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Total positivity in Markov structures
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 45
year: '2017'
...
---
_id: '1104'
abstract:
- lang: eng
  text: In the early visual system, cells of the same type perform the same computation
    in different places of the visual field. How these cells code together a complex
    visual scene is unclear. A common assumption is that cells of a single-type extract
    a single-stimulus feature to form a feature map, but this has rarely been observed
    directly. Using large-scale recordings in the rat retina, we show that a homogeneous
    population of fast OFF ganglion cells simultaneously encodes two radically different
    features of a visual scene. Cells close to a moving object code quasilinearly
    for its position, while distant cells remain largely invariant to the object's
    position and, instead, respond nonlinearly to changes in the object's speed. We
    develop a quantitative model that accounts for this effect and identify a disinhibitory
    circuit that mediates it. Ganglion cells of a single type thus do not code for
    one, but two features simultaneously. This richer, flexible neural map might also
    be present in other sensory systems.
article_number: '1964'
article_processing_charge: No
author:
- first_name: Stephane
  full_name: Deny, Stephane
  last_name: Deny
- first_name: Ulisse
  full_name: Ferrari, Ulisse
  last_name: Ferrari
- first_name: Emilie
  full_name: Mace, Emilie
  last_name: Mace
- first_name: Pierre
  full_name: Yger, Pierre
  last_name: Yger
- first_name: Romain
  full_name: Caplette, Romain
  last_name: Caplette
- first_name: Serge
  full_name: Picaud, Serge
  last_name: Picaud
- first_name: Gasper
  full_name: Tkacik, Gasper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkacik
  orcid: 0000-0002-6699-1455
- first_name: Olivier
  full_name: Marre, Olivier
  last_name: Marre
citation:
  ama: Deny S, Ferrari U, Mace E, et al. Multiplexed computations in retinal ganglion
    cells of a single type. <i>Nature Communications</i>. 2017;8(1). doi:<a href="https://doi.org/10.1038/s41467-017-02159-y">10.1038/s41467-017-02159-y</a>
  apa: Deny, S., Ferrari, U., Mace, E., Yger, P., Caplette, R., Picaud, S., … Marre,
    O. (2017). Multiplexed computations in retinal ganglion cells of a single type.
    <i>Nature Communications</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/s41467-017-02159-y">https://doi.org/10.1038/s41467-017-02159-y</a>
  chicago: Deny, Stephane, Ulisse Ferrari, Emilie Mace, Pierre Yger, Romain Caplette,
    Serge Picaud, Gašper Tkačik, and Olivier Marre. “Multiplexed Computations in Retinal
    Ganglion Cells of a Single Type.” <i>Nature Communications</i>. Nature Publishing
    Group, 2017. <a href="https://doi.org/10.1038/s41467-017-02159-y">https://doi.org/10.1038/s41467-017-02159-y</a>.
  ieee: S. Deny <i>et al.</i>, “Multiplexed computations in retinal ganglion cells
    of a single type,” <i>Nature Communications</i>, vol. 8, no. 1. Nature Publishing
    Group, 2017.
  ista: Deny S, Ferrari U, Mace E, Yger P, Caplette R, Picaud S, Tkačik G, Marre O.
    2017. Multiplexed computations in retinal ganglion cells of a single type. Nature
    Communications. 8(1), 1964.
  mla: Deny, Stephane, et al. “Multiplexed Computations in Retinal Ganglion Cells
    of a Single Type.” <i>Nature Communications</i>, vol. 8, no. 1, 1964, Nature Publishing
    Group, 2017, doi:<a href="https://doi.org/10.1038/s41467-017-02159-y">10.1038/s41467-017-02159-y</a>.
  short: S. Deny, U. Ferrari, E. Mace, P. Yger, R. Caplette, S. Picaud, G. Tkačik,
    O. Marre, Nature Communications 8 (2017).
date_created: 2018-12-11T11:50:10Z
date_published: 2017-12-06T00:00:00Z
date_updated: 2025-07-10T11:50:05Z
day: '06'
ddc:
- '571'
department:
- _id: GaTk
doi: 10.1038/s41467-017-02159-y
ec_funded: 1
external_id:
  isi:
  - '000417241200004'
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:16:06Z
  date_updated: 2018-12-12T10:16:06Z
  file_id: '5191'
  file_name: IST-2018-921-v1+1_s41467-017-02159-y.pdf
  file_size: 2872887
  relation: main_file
file_date_updated: 2018-12-12T10:16:06Z
fulldoi: https://doi.org/10.1038/s41467-017-02159-y
has_accepted_license: '1'
intvolume: '         8'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25CD3DD2-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '604102'
  name: Localization of ion channels and receptors by two and three-dimensional immunoelectron
    microscopic approaches
- _id: 254D1A94-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P 25651-N26
  name: Sensitivity to higher-order statistics in natural scenes
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Nature Publishing Group
publist_id: '6266'
pubrep_id: '921'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiplexed computations in retinal ganglion cells of a single type
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: 8
year: '2017'
...
---
_id: '11065'
abstract:
- lang: eng
  text: Premature aging disorders provide an opportunity to study the mechanisms that
    drive aging. In Hutchinson-Gilford progeria syndrome (HGPS), a mutant form of
    the nuclear scaffold protein lamin A distorts nuclei and sequesters nuclear proteins.
    We sought to investigate protein homeostasis in this disease. Here, we report
    a widespread increase in protein turnover in HGPS-derived cells compared to normal
    cells. We determine that global protein synthesis is elevated as a consequence
    of activated nucleoli and enhanced ribosome biogenesis in HGPS-derived fibroblasts.
    Depleting normal lamin A or inducing mutant lamin A expression are each sufficient
    to drive nucleolar expansion. We further show that nucleolar size correlates with
    donor age in primary fibroblasts derived from healthy individuals and that ribosomal
    RNA production increases with age, indicating that nucleolar size and activity
    can serve as aging biomarkers. While limiting ribosome biogenesis extends lifespan
    in several systems, we show that increased ribosome biogenesis and activity are
    a hallmark of premature aging.
article_number: '328'
article_processing_charge: No
article_type: original
author:
- first_name: Abigail
  full_name: Buchwalter, Abigail
  last_name: Buchwalter
- 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: Buchwalter A, Hetzer M. Nucleolar expansion and elevated protein translation
    in premature aging. <i>Nature Communications</i>. 2017;8. doi:<a href="https://doi.org/10.1038/s41467-017-00322-z">10.1038/s41467-017-00322-z</a>
  apa: Buchwalter, A., &#38; Hetzer, M. (2017). Nucleolar expansion and elevated protein
    translation in premature aging. <i>Nature Communications</i>. Springer Nature.
    <a href="https://doi.org/10.1038/s41467-017-00322-z">https://doi.org/10.1038/s41467-017-00322-z</a>
  chicago: Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated
    Protein Translation in Premature Aging.” <i>Nature Communications</i>. Springer
    Nature, 2017. <a href="https://doi.org/10.1038/s41467-017-00322-z">https://doi.org/10.1038/s41467-017-00322-z</a>.
  ieee: A. Buchwalter and M. Hetzer, “Nucleolar expansion and elevated protein translation
    in premature aging,” <i>Nature Communications</i>, vol. 8. Springer Nature, 2017.
  ista: Buchwalter A, Hetzer M. 2017. Nucleolar expansion and elevated protein translation
    in premature aging. Nature Communications. 8, 328.
  mla: Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated Protein
    Translation in Premature Aging.” <i>Nature Communications</i>, vol. 8, 328, Springer
    Nature, 2017, doi:<a href="https://doi.org/10.1038/s41467-017-00322-z">10.1038/s41467-017-00322-z</a>.
  short: A. Buchwalter, M. Hetzer, Nature Communications 8 (2017).
date_created: 2022-04-07T07:45:50Z
date_published: 2017-08-30T00:00:00Z
date_updated: 2024-10-14T11:20:12Z
day: '30'
doi: 10.1038/s41467-017-00322-z
extern: '1'
external_id:
  pmid:
  - '28855503'
fulldoi: https://doi.org/10.1038/s41467-017-00322-z
intvolume: '         8'
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-017-00322-z
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nucleolar expansion and elevated protein translation in premature aging
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '11066'
abstract:
- lang: eng
  text: Recent studies have shown that a subset of nucleoporins (Nups) can detach
    from the nuclear pore complex and move into the nuclear interior to regulate transcription.
    One such dynamic Nup, called Nup98, has been implicated in gene activation in
    healthy cells and has been shown to drive leukemogenesis when mutated in patients
    with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98
    binds predominantly to transcription start sites to recruit the Wdr82–Set1A/COMPASS
    (complex of proteins associated with Set1) complex, which is required for deposition
    of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98
    or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3
    at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated
    in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation
    of associated genes. Our findings establish a function of Nup98 in hematopoietic
    gene activation and provide mechanistic insight into which Nup98 leukemic fusion
    proteins promote AML.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias M.
  full_name: Franks, Tobias M.
  last_name: Franks
- first_name: Asako
  full_name: McCloskey, Asako
  last_name: McCloskey
- first_name: Maxim Nikolaievich
  full_name: Shokhirev, Maxim Nikolaievich
  last_name: Shokhirev
- first_name: Chris
  full_name: Benner, Chris
  last_name: Benner
- first_name: Annie
  full_name: Rathore, Annie
  last_name: Rathore
- 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: Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. Nup98
    recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation
    in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. 2017;31(22):2222-2234.
    doi:<a href="https://doi.org/10.1101/gad.306753.117">10.1101/gad.306753.117</a>
  apa: Franks, T. M., McCloskey, A., Shokhirev, M. N., Benner, C., Rathore, A., &#38;
    Hetzer, M. (2017). Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters
    to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38;
    Development</i>. Cold Spring Harbor Laboratory. <a href="https://doi.org/10.1101/gad.306753.117">https://doi.org/10.1101/gad.306753.117</a>
  chicago: Franks, Tobias M., Asako McCloskey, Maxim Nikolaievich Shokhirev, Chris
    Benner, Annie Rathore, and Martin Hetzer. “Nup98 Recruits the Wdr82–Set1A/COMPASS
    Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor
    Cells.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2017. <a
    href="https://doi.org/10.1101/gad.306753.117">https://doi.org/10.1101/gad.306753.117</a>.
  ieee: T. M. Franks, A. McCloskey, M. N. Shokhirev, C. Benner, A. Rathore, and M.
    Hetzer, “Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate
    H3K4 trimethylation in hematopoietic progenitor cells,” <i>Genes &#38; Development</i>,
    vol. 31, no. 22. Cold Spring Harbor Laboratory, pp. 2222–2234, 2017.
  ista: Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. 2017.
    Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation
    in hematopoietic progenitor cells. Genes &#38; Development. 31(22), 2222–2234.
  mla: Franks, Tobias M., et al. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to
    Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.”
    <i>Genes &#38; Development</i>, vol. 31, no. 22, Cold Spring Harbor Laboratory,
    2017, pp. 2222–34, doi:<a href="https://doi.org/10.1101/gad.306753.117">10.1101/gad.306753.117</a>.
  short: T.M. Franks, A. McCloskey, M.N. Shokhirev, C. Benner, A. Rathore, M. Hetzer,
    Genes &#38; Development 31 (2017) 2222–2234.
date_created: 2022-04-07T07:45:59Z
date_published: 2017-12-21T00:00:00Z
date_updated: 2024-10-14T11:20:24Z
day: '21'
doi: 10.1101/gad.306753.117
extern: '1'
external_id:
  pmid:
  - '29269482'
fulldoi: https://doi.org/10.1101/gad.306753.117
intvolume: '        31'
issue: '22'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/gad.306753.117
month: '12'
oa: 1
oa_version: Published Version
page: 2222-2234
pmid: 1
publication: Genes & Development
publication_identifier:
  issn:
  - 0890-9369
  - 1549-5477
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4
  trimethylation in hematopoietic progenitor cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2017'
...
---
_id: '11067'
abstract:
- lang: eng
  text: Neural progenitor cells (NeuPCs) possess a unique nuclear architecture that
    changes during differentiation. Nucleoporins are linked with cell-type-specific
    gene regulation, coupling physical changes in nuclear structure to transcriptional
    output; but, whether and how they coordinate with key fate-determining transcription
    factors is unclear. Here we show that the nucleoporin Nup153 interacts with Sox2
    in adult NeuPCs, where it is indispensable for their maintenance and controls
    neuronal differentiation. Genome-wide analyses show that Nup153 and Sox2 bind
    and co-regulate hundreds of genes. Binding of Nup153 to gene promoters or transcriptional
    end sites correlates with increased or decreased gene expression, respectively,
    and inhibiting Nup153 expression alters open chromatin configurations at its target
    genes, disrupts genomic localization of Sox2, and promotes differentiation in
    vitro and a gliogenic fate switch in vivo. Together, these findings reveal that
    nuclear structural proteins may exert bimodal transcriptional effects to control
    cell fate.
article_processing_charge: No
article_type: original
author:
- first_name: Tomohisa
  full_name: Toda, Tomohisa
  last_name: Toda
- first_name: Jonathan Y.
  full_name: Hsu, Jonathan Y.
  last_name: Hsu
- first_name: Sara B.
  full_name: Linker, Sara B.
  last_name: Linker
- first_name: Lauren
  full_name: Hu, Lauren
  last_name: Hu
- first_name: Simon T.
  full_name: Schafer, Simon T.
  last_name: Schafer
- first_name: Jerome
  full_name: Mertens, Jerome
  last_name: Mertens
- first_name: Filipe V.
  full_name: Jacinto, Filipe V.
  last_name: Jacinto
- first_name: Martin W
  full_name: HETZER, Martin W
  id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
  last_name: HETZER
  orcid: 0000-0002-2111-992X
- first_name: Fred H.
  full_name: Gage, Fred H.
  last_name: Gage
citation:
  ama: Toda T, Hsu JY, Linker SB, et al. Nup153 interacts with Sox2 to enable bimodal
    gene regulation and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>.
    2017;21(5):618-634.e7. doi:<a href="https://doi.org/10.1016/j.stem.2017.08.012">10.1016/j.stem.2017.08.012</a>
  apa: Toda, T., Hsu, J. Y., Linker, S. B., Hu, L., Schafer, S. T., Mertens, J., …
    Gage, F. H. (2017). Nup153 interacts with Sox2 to enable bimodal gene regulation
    and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>. Elsevier. <a
    href="https://doi.org/10.1016/j.stem.2017.08.012">https://doi.org/10.1016/j.stem.2017.08.012</a>
  chicago: Toda, Tomohisa, Jonathan Y. Hsu, Sara B. Linker, Lauren Hu, Simon T. Schafer,
    Jerome Mertens, Filipe V. Jacinto, Martin Hetzer, and Fred H. Gage. “Nup153 Interacts
    with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor
    Cells.” <i>Cell Stem Cell</i>. Elsevier, 2017. <a href="https://doi.org/10.1016/j.stem.2017.08.012">https://doi.org/10.1016/j.stem.2017.08.012</a>.
  ieee: T. Toda <i>et al.</i>, “Nup153 interacts with Sox2 to enable bimodal gene
    regulation and maintenance of neural progenitor cells,” <i>Cell Stem Cell</i>,
    vol. 21, no. 5. Elsevier, p. 618–634.e7, 2017.
  ista: Toda T, Hsu JY, Linker SB, Hu L, Schafer ST, Mertens J, Jacinto FV, Hetzer
    M, Gage FH. 2017. Nup153 interacts with Sox2 to enable bimodal gene regulation
    and maintenance of neural progenitor cells. Cell Stem Cell. 21(5), 618–634.e7.
  mla: Toda, Tomohisa, et al. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation
    and Maintenance of Neural Progenitor Cells.” <i>Cell Stem Cell</i>, vol. 21, no.
    5, Elsevier, 2017, p. 618–634.e7, doi:<a href="https://doi.org/10.1016/j.stem.2017.08.012">10.1016/j.stem.2017.08.012</a>.
  short: T. Toda, J.Y. Hsu, S.B. Linker, L. Hu, S.T. Schafer, J. Mertens, F.V. Jacinto,
    M. Hetzer, F.H. Gage, Cell Stem Cell 21 (2017) 618–634.e7.
date_created: 2022-04-07T07:46:12Z
date_published: 2017-11-02T00:00:00Z
date_updated: 2022-07-18T08:33:07Z
day: '02'
doi: 10.1016/j.stem.2017.08.012
extern: '1'
external_id:
  pmid:
  - '28919367'
fulldoi: https://doi.org/10.1016/j.stem.2017.08.012
intvolume: '        21'
issue: '5'
keyword:
- Cell Biology
- Genetics
- Molecular Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.stem.2017.08.012
month: '11'
oa: 1
oa_version: Published Version
page: 618-634.e7
pmid: 1
publication: Cell Stem Cell
publication_identifier:
  issn:
  - 1934-5909
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance
  of neural progenitor cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 21
year: '2017'
...
---
_id: '1107'
abstract:
- lang: eng
  text: The generation, migration, and differentiation of neurons requires the functional
    integrity of the microtubule cytoskeleton. Mutations in the tubulin gene family
    are known to cause various neurological diseases including lissencephaly, ocular
    motor disorders, polymicrogyria and amyotrophic lateral sclerosis. We have previously
    reported that mutations in TUBB5 cause microcephaly that is accompanied by severe
    intellectual impairment and motor delay. Here we present the characterization
    of a Tubb5 mouse model that allows for the conditional expression of the pathogenic
    E401K mutation. Homozygous knockin animals exhibit a severe reduction in brain
    size and in body weight. These animals do not show any significant impairment
    in general activity, anxiety, or in the acoustic startle response, however, present
    with notable defects in motor coordination. When assessed on the static rod apparatus
    mice took longer to orient and often lost their balance completely. Interestingly,
    mutant animals also showed defects in prepulse inhibition, a phenotype associated
    with sensorimotor gating and considered an endophenotype for schizophrenia. This
    study provides insight into the behavioral consequences of tubulin gene mutations.
acknowledgement: Austrian Science Fund (FWF) for funding this research [I914,P21092]
article_processing_charge: No
author:
- first_name: Martin
  full_name: Breuss, Martin
  last_name: Breuss
- first_name: Andi H
  full_name: Hansen, Andi H
  id: 38853E16-F248-11E8-B48F-1D18A9856A87
  last_name: Hansen
- first_name: Lukas
  full_name: Landler, Lukas
  last_name: Landler
- first_name: David
  full_name: Keays, David
  last_name: Keays
citation:
  ama: Breuss M, Hansen AH, Landler L, Keays D. Brain specific knockin of the pathogenic
    Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition.
    <i>Behavioural Brain Research</i>. 2017;323:47-55. doi:<a href="https://doi.org/10.1016/j.bbr.2017.01.029">10.1016/j.bbr.2017.01.029</a>
  apa: Breuss, M., Hansen, A. H., Landler, L., &#38; Keays, D. (2017). Brain specific
    knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination
    and prepulse inhibition. <i>Behavioural Brain Research</i>. Elsevier. <a href="https://doi.org/10.1016/j.bbr.2017.01.029">https://doi.org/10.1016/j.bbr.2017.01.029</a>
  chicago: Breuss, Martin, Andi H Hansen, Lukas Landler, and David Keays. “Brain Specific
    Knockin of the Pathogenic Tubb5 E401K Allele Causes Defects in Motor Coordination
    and Prepulse Inhibition.” <i>Behavioural Brain Research</i>. Elsevier, 2017. <a
    href="https://doi.org/10.1016/j.bbr.2017.01.029">https://doi.org/10.1016/j.bbr.2017.01.029</a>.
  ieee: M. Breuss, A. H. Hansen, L. Landler, and D. Keays, “Brain specific knockin
    of the pathogenic Tubb5 E401K allele causes defects in motor coordination and
    prepulse inhibition,” <i>Behavioural Brain Research</i>, vol. 323. Elsevier, pp.
    47–55, 2017.
  ista: Breuss M, Hansen AH, Landler L, Keays D. 2017. Brain specific knockin of the
    pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse
    inhibition. Behavioural Brain Research. 323, 47–55.
  mla: Breuss, Martin, et al. “Brain Specific Knockin of the Pathogenic Tubb5 E401K
    Allele Causes Defects in Motor Coordination and Prepulse Inhibition.” <i>Behavioural
    Brain Research</i>, vol. 323, Elsevier, 2017, pp. 47–55, doi:<a href="https://doi.org/10.1016/j.bbr.2017.01.029">10.1016/j.bbr.2017.01.029</a>.
  short: M. Breuss, A.H. Hansen, L. Landler, D. Keays, Behavioural Brain Research
    323 (2017) 47–55.
date_created: 2018-12-11T11:50:11Z
date_published: 2017-04-14T00:00:00Z
date_updated: 2023-09-20T11:37:25Z
day: '14'
ddc:
- '570'
- '571'
doi: 10.1016/j.bbr.2017.01.029
extern: '1'
external_id:
  isi:
  - '000397369100007'
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:03Z
  date_updated: 2018-12-12T10:12:03Z
  file_id: '4921'
  file_name: IST-2017-868-v1+1_1-s2.0-S0166432816309160-main.pdf
  file_size: 2291511
  relation: main_file
file_date_updated: 2018-12-12T10:12:03Z
fulldoi: https://doi.org/10.1016/j.bbr.2017.01.029
has_accepted_license: '1'
intvolume: '       323'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '04'
oa: 1
oa_version: Published Version
page: 47 - 55
publication: Behavioural Brain Research
publication_identifier:
  issn:
  - '01664328'
publication_status: published
publisher: Elsevier
publist_id: '6262'
pubrep_id: '868'
quality_controlled: '1'
status: public
title: Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects
  in motor coordination and prepulse inhibition
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 323
year: '2017'
...
