---
_id: '14850'
abstract:
- lang: eng
  text: Elaborate sexual signals are thought to have evolved and be maintained to
    serve as honest indicators of signaller quality. One measure of quality is health,
    which can be affected by parasite infection. Cnemaspis mysoriensis is a diurnal
    gecko that is often infested with ectoparasites in the wild, and males of this
    species express visual (coloured gular patches) and chemical (femoral gland secretions)
    traits that receivers could assess during social interactions. In this paper,
    we tested whether ectoparasites affect individual health, and whether signal quality
    is an indicator of ectoparasite levels. In wild lizards, we found that ectoparasite
    level was negatively correlated with body condition in both sexes. Moreover, some
    characteristics of both visual and chemical traits in males were strongly associated
    with ectoparasite levels. Specifically, males with higher ectoparasite levels
    had yellow gular patches with lower brightness and chroma, and chemical secretions
    with a lower proportion of aromatic compounds. We then determined whether ectoparasite
    levels in males influence female behaviour. Using sequential choice trials, wherein
    females were provided with either the visual or the chemical signals of wild-caught
    males that varied in ectoparasite level, we found that only chemical secretions
    evoked an elevated female response towards less parasitised males. Simultaneous
    choice trials in which females were exposed to the chemical secretions from males
    that varied in parasite level further confirmed a preference for males with lower
    parasites loads. Overall, we find that although health (body condition) or ectoparasite
    load can be honestly advertised through multiple modalities, the parasite-mediated
    female response is exclusively driven by chemical signals.</jats:p>
acknowledgement: "We thank Anuradha Batabyal and Shakilur Kabir for scientific discussions,
  and help with sampling and colour analyses. We thank Muralidhar and the central
  LCMS facility of the IISc for their technical support with the GCMS.\r\nResearch
  funding was provided by the Department of Science and Technology Fund for Improvement
  of S&T Infrastructure (DST-FIST), the Department of Biotechnology-Indian Institute
  of Science (DBT-IISc) partnership program and a Science and Engineering Research
  Board (SERB) grant to M.T. (EMR/2017/002228). Open Access funding provided by Indian
  Institute of Science. Deposited in PMC for immediate release."
article_number: jeb246217
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Arka
  full_name: Pal, Arka
  id: 6AAB2240-CA9A-11E9-9C1A-D9D1E5697425
  last_name: Pal
  orcid: 0000-0002-4530-8469
- first_name: Mihir
  full_name: Joshi, Mihir
  last_name: Joshi
- first_name: Maria
  full_name: Thaker, Maria
  last_name: Thaker
citation:
  ama: Pal A, Joshi M, Thaker M. Too much information? Males convey parasite levels
    using more signal modalities than females utilise. <i>Journal of Experimental
    Biology</i>. 2024;227(1). doi:<a href="https://doi.org/10.1242/jeb.246217">10.1242/jeb.246217</a>
  apa: Pal, A., Joshi, M., &#38; Thaker, M. (2024). Too much information? Males convey
    parasite levels using more signal modalities than females utilise. <i>Journal
    of Experimental Biology</i>. The Company of Biologists. <a href="https://doi.org/10.1242/jeb.246217">https://doi.org/10.1242/jeb.246217</a>
  chicago: Pal, Arka, Mihir Joshi, and Maria Thaker. “Too Much Information? Males
    Convey Parasite Levels Using More Signal Modalities than Females Utilise.” <i>Journal
    of Experimental Biology</i>. The Company of Biologists, 2024. <a href="https://doi.org/10.1242/jeb.246217">https://doi.org/10.1242/jeb.246217</a>.
  ieee: A. Pal, M. Joshi, and M. Thaker, “Too much information? Males convey parasite
    levels using more signal modalities than females utilise,” <i>Journal of Experimental
    Biology</i>, vol. 227, no. 1. The Company of Biologists, 2024.
  ista: Pal A, Joshi M, Thaker M. 2024. Too much information? Males convey parasite
    levels using more signal modalities than females utilise. Journal of Experimental
    Biology. 227(1), jeb246217.
  mla: Pal, Arka, et al. “Too Much Information? Males Convey Parasite Levels Using
    More Signal Modalities than Females Utilise.” <i>Journal of Experimental Biology</i>,
    vol. 227, no. 1, jeb246217, The Company of Biologists, 2024, doi:<a href="https://doi.org/10.1242/jeb.246217">10.1242/jeb.246217</a>.
  short: A. Pal, M. Joshi, M. Thaker, Journal of Experimental Biology 227 (2024).
corr_author: '1'
date_created: 2024-01-22T08:14:49Z
date_published: 2024-01-10T00:00:00Z
date_updated: 2025-09-04T11:50:21Z
day: '10'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.1242/jeb.246217
external_id:
  isi:
  - '001214515700016'
  pmid:
  - '38054353'
file:
- access_level: open_access
  checksum: 136325372f6f45abaa62a71e2d23bfb6
  content_type: application/pdf
  creator: dernst
  date_created: 2024-01-23T12:08:24Z
  date_updated: 2024-01-23T12:08:24Z
  file_id: '14877'
  file_name: 2024_JourExperimBiology_Pal.pdf
  file_size: 594128
  relation: main_file
  success: 1
file_date_updated: 2024-01-23T12:08:24Z
has_accepted_license: '1'
intvolume: '       227'
isi: 1
issue: '1'
keyword:
- Insect Science
- Molecular Biology
- Animal Science and Zoology
- Aquatic Science
- Physiology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Experimental Biology
publication_identifier:
  eissn:
  - 0022-0949
  issn:
  - 1477-9145
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
related_material:
  link:
  - relation: software
    url: https://github.com/arka-pal/Cnemaspis-SexualSignaling
scopus_import: '1'
status: public
title: Too much information? Males convey parasite levels using more signal modalities
  than females utilise
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 227
year: '2024'
...
---
_id: '12562'
abstract:
- lang: eng
  text: Presynaptic inputs determine the pattern of activation of postsynaptic neurons
    in a neural circuit. Molecular and genetic pathways that regulate the selective
    formation of subsets of presynaptic inputs are largely unknown, despite significant
    understanding of the general process of synaptogenesis. In this study, we have
    begun to identify such factors using the spinal monosynaptic stretch reflex circuit
    as a model system. In this neuronal circuit, Ia proprioceptive afferents establish
    monosynaptic connections with spinal motor neurons that project to the same muscle
    (termed homonymous connections) or muscles with related or synergistic function.
    However, monosynaptic connections are not formed with motor neurons innervating
    muscles with antagonistic functions. The ETS transcription factor ER81 (also known
    as ETV1) is expressed by all proprioceptive afferents, but only a small set of
    motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional
    mouse genetic techniques to eliminate Er81 expression selectively from motor neurons.
    We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive
    afferents conveying information from homonymous and synergistic muscles, with
    no change observed in the connectivity pattern from antagonistic proprioceptive
    afferents. In summary, these findings suggest a role for ER81 in defined motor
    neuron pools to control the assembly of specific presynaptic inputs and thereby
    influence the profile of activation of these motor neurons.
acknowledgement: The authors gratefully thank Dr. Silvia Arber, University of Basel
  and Friedrich Miescher Institute for Biomedical Research, for support and in whose
  lab the data were collected. For advice on statistical analysis, we thank Michael
  Bottomley from the Statistical Consulting Center, College of Science and Mathematics,
  Wright State University.
article_processing_charge: No
article_type: original
author:
- first_name: David R.
  full_name: Ladle, David R.
  last_name: Ladle
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
citation:
  ama: Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced
    monosynaptic inputs from proprioceptive sensory neurons. <i>Journal of Neurophysiology</i>.
    2023;129(3):501-512. doi:<a href="https://doi.org/10.1152/jn.00172.2022">10.1152/jn.00172.2022</a>
  apa: Ladle, D. R., &#38; Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons
    leads to reduced monosynaptic inputs from proprioceptive sensory neurons. <i>Journal
    of Neurophysiology</i>. American Physiological Society. <a href="https://doi.org/10.1152/jn.00172.2022">https://doi.org/10.1152/jn.00172.2022</a>
  chicago: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
    Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” <i>Journal
    of Neurophysiology</i>. American Physiological Society, 2023. <a href="https://doi.org/10.1152/jn.00172.2022">https://doi.org/10.1152/jn.00172.2022</a>.
  ieee: D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads
    to reduced monosynaptic inputs from proprioceptive sensory neurons,” <i>Journal
    of Neurophysiology</i>, vol. 129, no. 3. American Physiological Society, pp. 501–512,
    2023.
  ista: Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to
    reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology.
    129(3), 501–512.
  mla: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
    Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” <i>Journal
    of Neurophysiology</i>, vol. 129, no. 3, American Physiological Society, 2023,
    pp. 501–12, doi:<a href="https://doi.org/10.1152/jn.00172.2022">10.1152/jn.00172.2022</a>.
  short: D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512.
date_created: 2023-02-15T14:46:14Z
date_published: 2023-03-01T00:00:00Z
date_updated: 2024-10-21T06:01:28Z
day: '01'
department:
- _id: SiHi
doi: 10.1152/jn.00172.2022
external_id:
  isi:
  - '000957721600001'
  pmid:
  - '36695533'
intvolume: '       129'
isi: 1
issue: '3'
keyword:
- Physiology
- General Neuroscience
language:
- iso: eng
month: '03'
oa_version: None
page: 501-512
pmid: 1
publication: Journal of Neurophysiology
publication_identifier:
  eissn:
  - 1522-1598
  issn:
  - 0022-3077
publication_status: published
publisher: American Physiological Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from
  proprioceptive sensory neurons
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 129
year: '2023'
...
---
_id: '12747'
abstract:
- lang: eng
  text: Muscle degeneration is the most prevalent cause for frailty and dependency
    in inherited diseases and ageing. Elucidation of pathophysiological mechanisms,
    as well as effective treatments for muscle diseases, represents an important goal
    in improving human health. Here, we show that the lipid synthesis enzyme phosphatidylethanolamine
    cytidyltransferase (PCYT2/ECT) is critical to muscle health. Human deficiency
    in PCYT2 causes a severe disease with failure to thrive and progressive weakness.
    pcyt2-mutant zebrafish and muscle-specific Pcyt2-knockout mice recapitulate the
    participant phenotypes, with failure to thrive, progressive muscle weakness and
    accelerated ageing. Mechanistically, muscle Pcyt2 deficiency affects cellular
    bioenergetics and membrane lipid bilayer structure and stability. PCYT2 activity
    declines in ageing muscles of mice and humans, and adeno-associated virus-based
    delivery of PCYT2 ameliorates muscle weakness in Pcyt2-knockout and old mice,
    offering a therapy for individuals with a rare disease and muscle ageing. Thus,
    PCYT2 plays a fundamental and conserved role in vertebrate muscle health, linking
    PCYT2 and PCYT2-synthesized lipids to severe muscle dystrophy and ageing.
acknowledgement: 'The authors thank the participants and their families for participating
  in the study. We thank all members of our laboratories for helpful discussions.
  We are grateful to Vienna BioCenter Core Facilities: Mouse Phenotyping Unit, Histopathology
  Unit, Bioinformatics Unit, BioOptics Unit, Electron Microscopy Unit and Comparative
  Medicine Unit. We are grateful to the Lipidomics Facility, and K. Klavins and T.
  Hannich at the CeMM Research Center for Molecular Medicine of the Austrian Academy
  of Sciences for assistance with lipidomics analysis. We also thank T. Huan and A.
  Hui (UBC Vancouver) for mouse tissue and mitochondria lipidomics analysis. We thank
  A. Klymchenko (Laboratoire de Bioimagerie et Pathologies Université de Strasbourg,
  Strasbourg, France) for providing the NR12S probe. We are thankful to the Sen. Paul
  D. Wellstone Muscular Dystrophy Cooperative Specialized Research Center Viral Vector
  Core Facility for AAV6 production. We also thank K. P. Campbell and M. E. Anderson
  (University of Iowa, Carver College of Medicine) for advice on muscle tissue handling.
  We thank A. Al-Qassabi from the Sultan Qaboos University for the clinical assessment
  of the participants. D.C. and J.M.P. are supported by the Austrian Federal Ministry
  of Education, Science and Research, the Austrian Academy of Sciences, and the City
  of Vienna, and grants from the Austrian Science Fund (FWF) Wittgenstein award (Z
  271-B19), the T. von Zastrow Foundation, and a Canada 150 Research Chairs Program
  (F18-01336). J.S.C. is supported by grants RO1AR44533 and P50AR065139 from the US
  National Institutes of Health. C.K. is supported by a grant from the Agence Nationale
  de la Recherche (ANR-18-CE14-0007-01). A.V.K. is supported by European Union’s Horizon
  2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
  no. 67544, and an Austrian Science Fund (FWF; no P-33799). A.W. is supported by
  Austrian Research Promotion Agency (FFG) project no 867674. E.S. is supported by
  a SciLifeLab fellowship and Karolinska Institutet Foundation Grants. Work in the
  laboratory of G.S.-F. is supported by the Austrian Academy of Sciences, the European
  Research Council (ERC AdG 695214 GameofGates) and the Innovative Medicines Initiative
  2 Joint Undertaking (grant agreement no. 777372, ReSOLUTE). S.B., M.L. and R.Y.
  acknowledge the support of the Spastic Paraplegia Foundation.'
article_processing_charge: No
article_type: original
author:
- first_name: Domagoj
  full_name: Cikes, Domagoj
  last_name: Cikes
- first_name: Kareem
  full_name: Elsayad, Kareem
  last_name: Elsayad
- first_name: Erdinc
  full_name: Sezgin, Erdinc
  last_name: Sezgin
- first_name: Erika
  full_name: Koitai, Erika
  last_name: Koitai
- first_name: Torma
  full_name: Ferenc, Torma
  last_name: Ferenc
- first_name: Michael
  full_name: Orthofer, Michael
  last_name: Orthofer
- first_name: Rebecca
  full_name: Yarwood, Rebecca
  last_name: Yarwood
- first_name: Leonhard X.
  full_name: Heinz, Leonhard X.
  last_name: Heinz
- first_name: Vitaly
  full_name: Sedlyarov, Vitaly
  last_name: Sedlyarov
- first_name: Nasser
  full_name: Darwish-Miranda, Nasser
  id: 39CD9926-F248-11E8-B48F-1D18A9856A87
  last_name: Darwish-Miranda
  orcid: 0000-0002-8821-8236
- first_name: Adrian
  full_name: Taylor, Adrian
  last_name: Taylor
- first_name: Sophie
  full_name: Grapentine, Sophie
  last_name: Grapentine
- first_name: Fathiya
  full_name: al-Murshedi, Fathiya
  last_name: al-Murshedi
- first_name: Anne
  full_name: Abot, Anne
  last_name: Abot
- first_name: Adelheid
  full_name: Weidinger, Adelheid
  last_name: Weidinger
- first_name: Candice
  full_name: Kutchukian, Candice
  last_name: Kutchukian
- first_name: Colline
  full_name: Sanchez, Colline
  last_name: Sanchez
- first_name: Shane J. F.
  full_name: Cronin, Shane J. F.
  last_name: Cronin
- first_name: Maria
  full_name: Novatchkova, Maria
  last_name: Novatchkova
- first_name: Anoop
  full_name: Kavirayani, Anoop
  last_name: Kavirayani
- first_name: Thomas
  full_name: Schuetz, Thomas
  last_name: Schuetz
- first_name: Bernhard
  full_name: Haubner, Bernhard
  last_name: Haubner
- first_name: Lisa
  full_name: Haas, Lisa
  last_name: Haas
- first_name: Astrid
  full_name: Hagelkruys, Astrid
  last_name: Hagelkruys
- first_name: Suzanne
  full_name: Jackowski, Suzanne
  last_name: Jackowski
- first_name: Andrey
  full_name: Kozlov, Andrey
  last_name: Kozlov
- first_name: Vincent
  full_name: Jacquemond, Vincent
  last_name: Jacquemond
- first_name: Claude
  full_name: Knauf, Claude
  last_name: Knauf
- first_name: Giulio
  full_name: Superti-Furga, Giulio
  last_name: Superti-Furga
- first_name: Eric
  full_name: Rullman, Eric
  last_name: Rullman
- first_name: Thomas
  full_name: Gustafsson, Thomas
  last_name: Gustafsson
- first_name: John
  full_name: McDermot, John
  last_name: McDermot
- first_name: Martin
  full_name: Lowe, Martin
  last_name: Lowe
- first_name: Zsolt
  full_name: Radak, Zsolt
  last_name: Radak
- first_name: Jeffrey S.
  full_name: Chamberlain, Jeffrey S.
  last_name: Chamberlain
- first_name: Marica
  full_name: Bakovic, Marica
  last_name: Bakovic
- first_name: Siddharth
  full_name: Banka, Siddharth
  last_name: Banka
- first_name: Josef M.
  full_name: Penninger, Josef M.
  last_name: Penninger
citation:
  ama: Cikes D, Elsayad K, Sezgin E, et al. PCYT2-regulated lipid biosynthesis is
    critical to muscle health and ageing. <i>Nature Metabolism</i>. 2023;5:495-515.
    doi:<a href="https://doi.org/10.1038/s42255-023-00766-2">10.1038/s42255-023-00766-2</a>
  apa: Cikes, D., Elsayad, K., Sezgin, E., Koitai, E., Ferenc, T., Orthofer, M., …
    Penninger, J. M. (2023). PCYT2-regulated lipid biosynthesis is critical to muscle
    health and ageing. <i>Nature Metabolism</i>. Springer Nature. <a href="https://doi.org/10.1038/s42255-023-00766-2">https://doi.org/10.1038/s42255-023-00766-2</a>
  chicago: Cikes, Domagoj, Kareem Elsayad, Erdinc Sezgin, Erika Koitai, Torma Ferenc,
    Michael Orthofer, Rebecca Yarwood, et al. “PCYT2-Regulated Lipid Biosynthesis
    Is Critical to Muscle Health and Ageing.” <i>Nature Metabolism</i>. Springer Nature,
    2023. <a href="https://doi.org/10.1038/s42255-023-00766-2">https://doi.org/10.1038/s42255-023-00766-2</a>.
  ieee: D. Cikes <i>et al.</i>, “PCYT2-regulated lipid biosynthesis is critical to
    muscle health and ageing,” <i>Nature Metabolism</i>, vol. 5. Springer Nature,
    pp. 495–515, 2023.
  ista: Cikes D, Elsayad K, Sezgin E, Koitai E, Ferenc T, Orthofer M, Yarwood R, Heinz
    LX, Sedlyarov V, Darwish-Miranda N, Taylor A, Grapentine S, al-Murshedi F, Abot
    A, Weidinger A, Kutchukian C, Sanchez C, Cronin SJF, Novatchkova M, Kavirayani
    A, Schuetz T, Haubner B, Haas L, Hagelkruys A, Jackowski S, Kozlov A, Jacquemond
    V, Knauf C, Superti-Furga G, Rullman E, Gustafsson T, McDermot J, Lowe M, Radak
    Z, Chamberlain JS, Bakovic M, Banka S, Penninger JM. 2023. PCYT2-regulated lipid
    biosynthesis is critical to muscle health and ageing. Nature Metabolism. 5, 495–515.
  mla: Cikes, Domagoj, et al. “PCYT2-Regulated Lipid Biosynthesis Is Critical to Muscle
    Health and Ageing.” <i>Nature Metabolism</i>, vol. 5, Springer Nature, 2023, pp.
    495–515, doi:<a href="https://doi.org/10.1038/s42255-023-00766-2">10.1038/s42255-023-00766-2</a>.
  short: D. Cikes, K. Elsayad, E. Sezgin, E. Koitai, T. Ferenc, M. Orthofer, R. Yarwood,
    L.X. Heinz, V. Sedlyarov, N. Darwish-Miranda, A. Taylor, S. Grapentine, F. al-Murshedi,
    A. Abot, A. Weidinger, C. Kutchukian, C. Sanchez, S.J.F. Cronin, M. Novatchkova,
    A. Kavirayani, T. Schuetz, B. Haubner, L. Haas, A. Hagelkruys, S. Jackowski, A.
    Kozlov, V. Jacquemond, C. Knauf, G. Superti-Furga, E. Rullman, T. Gustafsson,
    J. McDermot, M. Lowe, Z. Radak, J.S. Chamberlain, M. Bakovic, S. Banka, J.M. Penninger,
    Nature Metabolism 5 (2023) 495–515.
date_created: 2023-03-23T12:58:43Z
date_published: 2023-03-20T00:00:00Z
date_updated: 2023-11-28T07:31:33Z
day: '20'
department:
- _id: Bio
doi: 10.1038/s42255-023-00766-2
external_id:
  isi:
  - '000992064000002'
  pmid:
  - '36941451'
intvolume: '         5'
isi: 1
keyword:
- Cell Biology
- Physiology (medical)
- Endocrinology
- Diabetes and Metabolism
- Internal Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/2022.03.02.482658
month: '03'
oa: 1
oa_version: Preprint
page: 495-515
pmid: 1
publication: Nature Metabolism
publication_identifier:
  issn:
  - 2522-5812
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  link:
  - relation: erratum
    url: https://doi.org/10.1038/s42255-023-00791-1
scopus_import: '1'
status: public
title: PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2023'
...
---
_id: '12186'
abstract:
- lang: eng
  text: Activation of cell-surface and intracellular receptor-mediated immunity results
    in rapid transcriptional reprogramming that underpins disease resistance. However,
    the mechanisms by which co-activation of both immune systems lead to transcriptional
    changes are not clear. Here, we combine RNA-seq and ATAC-seq to define changes
    in gene expression and chromatin accessibility. Activation of cell-surface or
    intracellular receptor-mediated immunity, or both, increases chromatin accessibility
    at induced defence genes. Analysis of ATAC-seq and RNA-seq data combined with
    publicly available information on transcription factor DNA-binding motifs enabled
    comparison of individual gene regulatory networks activated by cell-surface or
    intracellular receptor-mediated immunity, or by both. These results and analyses
    reveal overlapping and conserved transcriptional regulatory mechanisms between
    the two immune systems.
acknowledgement: "We thank the Gatsby Foundation (UK) for funding to the JDGJ laboratory.
  PD acknowledges support from the European Union’s Horizon 2020 Research and Innovation
  Program under Marie Skłodowska Curie Actions (grant agreement: 656243) and a Future
  Leader Fellowship from the Biotechnology and Biological Sciences Research Council
  (BBSRC) (grant agreement: BB/R012172/1). TS, RKS, DM, and JDGJ were supported by
  the Gatsby Foundation funding to the\r\nSainsbury Laboratory. NMP and KV were supported
  by a BOF grant from Ghent University (grant agreement: BOF24Y2019001901). WG and
  RZ were supported by the Scottish Government Rural and Environment Science and Analytical
  Services division (RESAS), and RZ also acknowledges the support from a BBSRC Bioinformatics
  and Biological Resources Fund (grant agreement: BB/S020160/1).BPMN was supported
  by the Norwich Research Park (NRP) Biosciences Doctoral Training Partnership (DTP)
  funded by the BBSRC (grant agreement: BB/M011216/1). SH and XF were supported by
  a BBSRC Responsive Mode grant (grant agreement: BB/S009620/1) and a European Research
  Council Starting grant ‘SexMeth’ (grant agreement: 804981). CL was supported by
  Deutsche Forschungsgemeinschaft (grant agreement: LI 2862/4). "
article_processing_charge: No
article_type: original
author:
- first_name: Pingtao
  full_name: Ding, Pingtao
  last_name: Ding
- first_name: Toshiyuki
  full_name: Sakai, Toshiyuki
  last_name: Sakai
- first_name: Ram
  full_name: Krishna Shrestha, Ram
  last_name: Krishna Shrestha
- first_name: Nicolas
  full_name: Manosalva Perez, Nicolas
  last_name: Manosalva Perez
- first_name: Wenbin
  full_name: Guo, Wenbin
  last_name: Guo
- first_name: Bruno Pok Man
  full_name: Ngou, Bruno Pok Man
  last_name: Ngou
- first_name: Shengbo
  full_name: He, Shengbo
  last_name: He
- first_name: Chang
  full_name: Liu, Chang
  last_name: Liu
- first_name: Xiaoqi
  full_name: Feng, Xiaoqi
  id: e0164712-22ee-11ed-b12a-d80fcdf35958
  last_name: Feng
  orcid: 0000-0002-4008-1234
- first_name: Runxuan
  full_name: Zhang, Runxuan
  last_name: Zhang
- first_name: Klaas
  full_name: Vandepoele, Klaas
  last_name: Vandepoele
- first_name: Dan
  full_name: MacLean, Dan
  last_name: MacLean
- first_name: Jonathan D G
  full_name: Jones, Jonathan D G
  last_name: Jones
citation:
  ama: Ding P, Sakai T, Krishna Shrestha R, et al. Chromatin accessibility landscapes
    activated by cell-surface and intracellular immune receptors. <i>Journal of Experimental
    Botany</i>. 2021;72(22):7927-7941. doi:<a href="https://doi.org/10.1093/jxb/erab373">10.1093/jxb/erab373</a>
  apa: Ding, P., Sakai, T., Krishna Shrestha, R., Manosalva Perez, N., Guo, W., Ngou,
    B. P. M., … Jones, J. D. G. (2021). Chromatin accessibility landscapes activated
    by cell-surface and intracellular immune receptors. <i>Journal of Experimental
    Botany</i>. Oxford University Press. <a href="https://doi.org/10.1093/jxb/erab373">https://doi.org/10.1093/jxb/erab373</a>
  chicago: Ding, Pingtao, Toshiyuki Sakai, Ram Krishna Shrestha, Nicolas Manosalva
    Perez, Wenbin Guo, Bruno Pok Man Ngou, Shengbo He, et al. “Chromatin Accessibility
    Landscapes Activated by Cell-Surface and Intracellular Immune Receptors.” <i>Journal
    of Experimental Botany</i>. Oxford University Press, 2021. <a href="https://doi.org/10.1093/jxb/erab373">https://doi.org/10.1093/jxb/erab373</a>.
  ieee: P. Ding <i>et al.</i>, “Chromatin accessibility landscapes activated by cell-surface
    and intracellular immune receptors,” <i>Journal of Experimental Botany</i>, vol.
    72, no. 22. Oxford University Press, pp. 7927–7941, 2021.
  ista: Ding P, Sakai T, Krishna Shrestha R, Manosalva Perez N, Guo W, Ngou BPM, He
    S, Liu C, Feng X, Zhang R, Vandepoele K, MacLean D, Jones JDG. 2021. Chromatin
    accessibility landscapes activated by cell-surface and intracellular immune receptors.
    Journal of Experimental Botany. 72(22), 7927–7941.
  mla: Ding, Pingtao, et al. “Chromatin Accessibility Landscapes Activated by Cell-Surface
    and Intracellular Immune Receptors.” <i>Journal of Experimental Botany</i>, vol.
    72, no. 22, Oxford University Press, 2021, pp. 7927–41, doi:<a href="https://doi.org/10.1093/jxb/erab373">10.1093/jxb/erab373</a>.
  short: P. Ding, T. Sakai, R. Krishna Shrestha, N. Manosalva Perez, W. Guo, B.P.M.
    Ngou, S. He, C. Liu, X. Feng, R. Zhang, K. Vandepoele, D. MacLean, J.D.G. Jones,
    Journal of Experimental Botany 72 (2021) 7927–7941.
date_created: 2023-01-16T09:14:35Z
date_published: 2021-08-13T00:00:00Z
date_updated: 2023-05-08T11:01:18Z
day: '13'
department:
- _id: XiFe
doi: 10.1093/jxb/erab373
extern: '1'
external_id:
  pmid:
  - '34387350'
intvolume: '        72'
issue: '22'
keyword:
- Plant Science
- Physiology
language:
- iso: eng
month: '08'
oa_version: None
page: 7927-7941
pmid: 1
publication: Journal of Experimental Botany
publication_identifier:
  issn:
  - 0022-0957
  - 1460-2431
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Chromatin accessibility landscapes activated by cell-surface and intracellular
  immune receptors
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 72
year: '2021'
...
---
_id: '8097'
abstract:
- lang: eng
  text: 'Antibiotics that interfere with translation, when combined, interact in diverse
    and difficult-to-predict ways. Here, we explain these interactions by "translation
    bottlenecks": points in the translation cycle where antibiotics block ribosomal
    progression. To elucidate the underlying mechanisms of drug interactions between
    translation inhibitors, we generate translation bottlenecks genetically using
    inducible control of translation factors that regulate well-defined translation
    cycle steps. These perturbations accurately mimic antibiotic action and drug interactions,
    supporting that the interplay of different translation bottlenecks causes these
    interactions. We further show that growth laws, combined with drug uptake and
    binding kinetics, enable the direct prediction of a large fraction of observed
    interactions, yet fail to predict suppression. However, varying two translation
    bottlenecks simultaneously supports that dense traffic of ribosomes and competition
    for translation factors account for the previously unexplained suppression. These
    results highlight the importance of "continuous epistasis" in bacterial physiology.'
acknowledged_ssus:
- _id: LifeSc
article_processing_charge: No
author:
- first_name: Bor
  full_name: Kavcic, Bor
  id: 350F91D2-F248-11E8-B48F-1D18A9856A87
  last_name: Kavcic
  orcid: 0000-0001-6041-254X
citation:
  ama: Kavcic B. Analysis scripts and research data for the paper “Mechanisms of drug
    interactions between translation-inhibiting antibiotics.” 2020. doi:<a href="https://doi.org/10.15479/AT:ISTA:8097">10.15479/AT:ISTA:8097</a>
  apa: Kavcic, B. (2020). Analysis scripts and research data for the paper “Mechanisms
    of drug interactions between translation-inhibiting antibiotics.” Institute of
    Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:8097">https://doi.org/10.15479/AT:ISTA:8097</a>
  chicago: Kavcic, Bor. “Analysis Scripts and Research Data for the Paper ‘Mechanisms
    of Drug Interactions between Translation-Inhibiting Antibiotics.’” Institute of
    Science and Technology Austria, 2020. <a href="https://doi.org/10.15479/AT:ISTA:8097">https://doi.org/10.15479/AT:ISTA:8097</a>.
  ieee: B. Kavcic, “Analysis scripts and research data for the paper ‘Mechanisms of
    drug interactions between translation-inhibiting antibiotics.’” Institute of Science
    and Technology Austria, 2020.
  ista: Kavcic B. 2020. Analysis scripts and research data for the paper ‘Mechanisms
    of drug interactions between translation-inhibiting antibiotics’, Institute of
    Science and Technology Austria, <a href="https://doi.org/10.15479/AT:ISTA:8097">10.15479/AT:ISTA:8097</a>.
  mla: Kavcic, Bor. <i>Analysis Scripts and Research Data for the Paper “Mechanisms
    of Drug Interactions between Translation-Inhibiting Antibiotics.”</i> Institute
    of Science and Technology Austria, 2020, doi:<a href="https://doi.org/10.15479/AT:ISTA:8097">10.15479/AT:ISTA:8097</a>.
  short: B. Kavcic, (2020).
contributor:
- contributor_type: research_group
  first_name: Gašper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkačik
  orcid: 0000-0002-6699-1455
- contributor_type: research_group
  first_name: Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
date_created: 2020-07-06T20:40:19Z
date_published: 2020-07-15T00:00:00Z
date_updated: 2024-02-21T12:40:51Z
day: '15'
department:
- _id: GaTk
doi: 10.15479/AT:ISTA:8097
file:
- access_level: open_access
  checksum: 5c321dbbb6d4b3c85da786fd3ebbdc98
  content_type: application/zip
  creator: bkavcic
  date_created: 2020-07-06T20:38:27Z
  date_updated: 2020-07-14T12:48:09Z
  file_id: '8098'
  file_name: natComm_2020_scripts.zip
  file_size: 255770756
  relation: main_file
file_date_updated: 2020-07-14T12:48:09Z
has_accepted_license: '1'
keyword:
- Escherichia coli
- antibiotic combinations
- translation
- growth laws
- drug interactions
- bacterial physiology
- translation inhibitors
month: '07'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Analysis scripts and research data for the paper "Mechanisms of drug interactions
  between translation-inhibiting antibiotics"
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: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '8402'
abstract:
- lang: eng
  text: "Background: The mitochondrial pyruvate carrier (MPC) plays a central role
    in energy metabolism by transporting pyruvate across the inner mitochondrial membrane.
    Its heterodimeric composition and homology to SWEET and semiSWEET transporters
    set the MPC apart from the canonical mitochondrial carrier family (named MCF or
    SLC25). The import of the canonical carriers is mediated by the carrier translocase
    of the inner membrane (TIM22) pathway and is dependent on their structure, which
    features an even number of transmembrane segments and both termini in the intermembrane
    space. The import pathway of MPC proteins has not been elucidated. The odd number
    of transmembrane segments and positioning of the N-terminus in the matrix argues
    against an import via the TIM22 carrier pathway but favors an import via the flexible
    presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways
    of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible
    presequence pathway, yeast MPC proteins with an odd number of transmembrane segments
    and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor
    Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones
    MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic
    motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions:
    The carrier pathway can import paired and non-paired transmembrane helices and
    translocate N-termini to either side of the mitochondrial inner membrane, revealing
    an unexpected versatility of the mitochondrial import pathway for non-cleavable
    inner membrane proteins."
article_number: '2'
article_processing_charge: No
article_type: original
author:
- first_name: Heike
  full_name: Rampelt, Heike
  last_name: Rampelt
- first_name: Iva
  full_name: Sucec, Iva
  last_name: Sucec
- first_name: Beate
  full_name: Bersch, Beate
  last_name: Bersch
- first_name: Patrick
  full_name: Horten, Patrick
  last_name: Horten
- first_name: Inge
  full_name: Perschil, Inge
  last_name: Perschil
- first_name: Jean-Claude
  full_name: Martinou, Jean-Claude
  last_name: Martinou
- first_name: Martin
  full_name: van der Laan, Martin
  last_name: van der Laan
- first_name: Nils
  full_name: Wiedemann, Nils
  last_name: Wiedemann
- first_name: Paul
  full_name: Schanda, Paul
  id: 7B541462-FAF6-11E9-A490-E8DFE5697425
  last_name: Schanda
  orcid: 0000-0002-9350-7606
- first_name: Nikolaus
  full_name: Pfanner, Nikolaus
  last_name: Pfanner
citation:
  ama: Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports
    non-canonical substrates with an odd number of transmembrane segments. <i>BMC
    Biology</i>. 2020;18. doi:<a href="https://doi.org/10.1186/s12915-019-0733-6">10.1186/s12915-019-0733-6</a>
  apa: Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C.,
    … Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical
    substrates with an odd number of transmembrane segments. <i>BMC Biology</i>. Springer
    Nature. <a href="https://doi.org/10.1186/s12915-019-0733-6">https://doi.org/10.1186/s12915-019-0733-6</a>
  chicago: Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil,
    Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus
    Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates
    with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>. Springer Nature,
    2020. <a href="https://doi.org/10.1186/s12915-019-0733-6">https://doi.org/10.1186/s12915-019-0733-6</a>.
  ieee: H. Rampelt <i>et al.</i>, “The mitochondrial carrier pathway transports non-canonical
    substrates with an odd number of transmembrane segments,” <i>BMC Biology</i>,
    vol. 18. Springer Nature, 2020.
  ista: Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der
    Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway
    transports non-canonical substrates with an odd number of transmembrane segments.
    BMC Biology. 18, 2.
  mla: Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical
    Substrates with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>,
    vol. 18, 2, Springer Nature, 2020, doi:<a href="https://doi.org/10.1186/s12915-019-0733-6">10.1186/s12915-019-0733-6</a>.
  short: H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou,
    M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020).
date_created: 2020-09-17T10:26:53Z
date_published: 2020-01-06T00:00:00Z
date_updated: 2024-10-15T13:23:11Z
day: '06'
doi: 10.1186/s12915-019-0733-6
extern: '1'
external_id:
  pmid:
  - '31907035'
intvolume: '        18'
keyword:
- Biotechnology
- Plant Science
- General Biochemistry
- Genetics and Molecular Biology
- Developmental Biology
- Cell Biology
- Physiology
- Ecology
- Evolution
- Behavior and Systematics
- Structural Biology
- General Agricultural and Biological Sciences
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1186/s12915-019-0733-6
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: BMC Biology
publication_identifier:
  issn:
  - 1741-7007
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: The mitochondrial carrier pathway transports non-canonical substrates with
  an odd number of transmembrane segments
type: journal_article
user_id: 0043cee0-e5fc-11ee-9736-f83bc23afbf0
volume: 18
year: '2020'
...
---
_id: '8930'
abstract:
- lang: eng
  text: Phenomenological relations such as Ohm’s or Fourier’s law have a venerable
    history in physics but are still scarce in biology. This situation restrains predictive
    theory. Here, we build on bacterial “growth laws,” which capture physiological
    feedback between translation and cell growth, to construct a minimal biophysical
    model for the combined action of ribosome-targeting antibiotics. Our model predicts
    drug interactions like antagonism or synergy solely from responses to individual
    drugs. We provide analytical results for limiting cases, which agree well with
    numerical results. We systematically refine the model by including direct physical
    interactions of different antibiotics on the ribosome. In a limiting case, our
    model provides a mechanistic underpinning for recent predictions of higher-order
    interactions that were derived using entropy maximization. We further refine the
    model to include the effects of antibiotics that mimic starvation and the presence
    of resistance genes. We describe the impact of a starvation-mimicking antibiotic
    on drug interactions analytically and verify it experimentally. Our extended model
    suggests a change in the type of drug interaction that depends on the strength
    of resistance, which challenges established rescaling paradigms. We experimentally
    show that the presence of unregulated resistance genes can lead to altered drug
    interaction, which agrees with the prediction of the model. While minimal, the
    model is readily adaptable and opens the door to predicting interactions of second
    and higher-order in a broad range of biological systems.
article_processing_charge: No
author:
- first_name: Bor
  full_name: Kavcic, Bor
  id: 350F91D2-F248-11E8-B48F-1D18A9856A87
  last_name: Kavcic
  orcid: 0000-0001-6041-254X
citation:
  ama: Kavcic B. Analysis scripts and research data for the paper “Minimal biophysical
    model of combined antibiotic action.” 2020. doi:<a href="https://doi.org/10.15479/AT:ISTA:8930">10.15479/AT:ISTA:8930</a>
  apa: Kavcic, B. (2020). Analysis scripts and research data for the paper “Minimal
    biophysical model of combined antibiotic action.” Institute of Science and Technology
    Austria. <a href="https://doi.org/10.15479/AT:ISTA:8930">https://doi.org/10.15479/AT:ISTA:8930</a>
  chicago: Kavcic, Bor. “Analysis Scripts and Research Data for the Paper ‘Minimal
    Biophysical Model of Combined Antibiotic Action.’” Institute of Science and Technology
    Austria, 2020. <a href="https://doi.org/10.15479/AT:ISTA:8930">https://doi.org/10.15479/AT:ISTA:8930</a>.
  ieee: B. Kavcic, “Analysis scripts and research data for the paper ‘Minimal biophysical
    model of combined antibiotic action.’” Institute of Science and Technology Austria,
    2020.
  ista: Kavcic B. 2020. Analysis scripts and research data for the paper ‘Minimal
    biophysical model of combined antibiotic action’, Institute of Science and Technology
    Austria, <a href="https://doi.org/10.15479/AT:ISTA:8930">10.15479/AT:ISTA:8930</a>.
  mla: Kavcic, Bor. <i>Analysis Scripts and Research Data for the Paper “Minimal Biophysical
    Model of Combined Antibiotic Action.”</i> Institute of Science and Technology
    Austria, 2020, doi:<a href="https://doi.org/10.15479/AT:ISTA:8930">10.15479/AT:ISTA:8930</a>.
  short: B. Kavcic, (2020).
contributor:
- contributor_type: supervisor
  first_name: Gašper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkačik
  orcid: 0000-0002-6699-1455
- contributor_type: supervisor
  first_name: Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
corr_author: '1'
date_created: 2020-12-09T15:04:02Z
date_published: 2020-12-10T00:00:00Z
date_updated: 2025-06-12T06:33:18Z
day: '10'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.15479/AT:ISTA:8930
file:
- access_level: open_access
  checksum: 60a818edeffaa7da1ebf5f8fbea9ba18
  content_type: application/zip
  creator: bkavcic
  date_created: 2020-12-09T15:00:19Z
  date_updated: 2020-12-09T15:00:19Z
  file_id: '8932'
  file_name: PLoSCompBiol2020_datarep.zip
  file_size: 315494370
  relation: main_file
  success: 1
file_date_updated: 2020-12-09T15:00:19Z
has_accepted_license: '1'
keyword:
- Escherichia coli
- antibiotic combinations
- translation
- growth laws
- drug interactions
- bacterial physiology
- translation inhibitors
month: '12'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '8997'
    relation: used_in_publication
    status: public
status: public
title: Analysis scripts and research data for the paper "Minimal biophysical model
  of combined antibiotic action"
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '11062'
abstract:
- lang: eng
  text: Most neurons are not replaced during an animal’s lifetime. This nondividing
    state is characterized by extreme longevity and age-dependent decline of key regulatory
    proteins. To study the lifespans of cells and proteins in adult tissues, we combined
    isotope labeling of mice with a hybrid imaging method (MIMS-EM). Using 15N mapping,
    we show that liver and pancreas are composed of cells with vastly different ages,
    many as old as the animal. Strikingly, we also found that a subset of fibroblasts
    and endothelial cells, both known for their replicative potential, are characterized
    by the absence of cell division during adulthood. In addition, we show that the
    primary cilia of beta cells and neurons contains different structural regions
    with vastly different lifespans. Based on these results, we propose that age mosaicism
    across multiple scales is a fundamental principle of adult tissue, cell, and protein
    complex organization.
article_processing_charge: No
article_type: original
author:
- first_name: Rafael
  full_name: Arrojo e Drigo, Rafael
  last_name: Arrojo e Drigo
- first_name: Varda
  full_name: Lev-Ram, Varda
  last_name: Lev-Ram
- first_name: Swati
  full_name: Tyagi, Swati
  last_name: Tyagi
- first_name: Ranjan
  full_name: Ramachandra, Ranjan
  last_name: Ramachandra
- first_name: Thomas
  full_name: Deerinck, Thomas
  last_name: Deerinck
- first_name: Eric
  full_name: Bushong, Eric
  last_name: Bushong
- first_name: Sebastien
  full_name: Phan, Sebastien
  last_name: Phan
- first_name: Victoria
  full_name: Orphan, Victoria
  last_name: Orphan
- first_name: Claude
  full_name: Lechene, Claude
  last_name: Lechene
- first_name: Mark H.
  full_name: Ellisman, Mark H.
  last_name: Ellisman
- first_name: Martin W
  full_name: HETZER, Martin W
  id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
  last_name: HETZER
  orcid: 0000-0002-2111-992X
citation:
  ama: Arrojo e Drigo R, Lev-Ram V, Tyagi S, et al. Age mosaicism across multiple
    scales in adult tissues. <i>Cell Metabolism</i>. 2019;30(2):343-351.e3. doi:<a
    href="https://doi.org/10.1016/j.cmet.2019.05.010">10.1016/j.cmet.2019.05.010</a>
  apa: Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T.,
    Bushong, E., … Hetzer, M. (2019). Age mosaicism across multiple scales in adult
    tissues. <i>Cell Metabolism</i>. Elsevier. <a href="https://doi.org/10.1016/j.cmet.2019.05.010">https://doi.org/10.1016/j.cmet.2019.05.010</a>
  chicago: Arrojo e Drigo, Rafael, Varda Lev-Ram, Swati Tyagi, Ranjan Ramachandra,
    Thomas Deerinck, Eric Bushong, Sebastien Phan, et al. “Age Mosaicism across Multiple
    Scales in Adult Tissues.” <i>Cell Metabolism</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.cmet.2019.05.010">https://doi.org/10.1016/j.cmet.2019.05.010</a>.
  ieee: R. Arrojo e Drigo <i>et al.</i>, “Age mosaicism across multiple scales in
    adult tissues,” <i>Cell Metabolism</i>, vol. 30, no. 2. Elsevier, p. 343–351.e3,
    2019.
  ista: Arrojo e Drigo R, Lev-Ram V, Tyagi S, Ramachandra R, Deerinck T, Bushong E,
    Phan S, Orphan V, Lechene C, Ellisman MH, Hetzer M. 2019. Age mosaicism across
    multiple scales in adult tissues. Cell Metabolism. 30(2), 343–351.e3.
  mla: Arrojo e Drigo, Rafael, et al. “Age Mosaicism across Multiple Scales in Adult
    Tissues.” <i>Cell Metabolism</i>, vol. 30, no. 2, Elsevier, 2019, p. 343–351.e3,
    doi:<a href="https://doi.org/10.1016/j.cmet.2019.05.010">10.1016/j.cmet.2019.05.010</a>.
  short: R. Arrojo e Drigo, V. Lev-Ram, S. Tyagi, R. Ramachandra, T. Deerinck, E.
    Bushong, S. Phan, V. Orphan, C. Lechene, M.H. Ellisman, M. Hetzer, Cell Metabolism
    30 (2019) 343–351.e3.
date_created: 2022-04-07T07:45:21Z
date_published: 2019-08-06T00:00:00Z
date_updated: 2025-12-15T10:02:11Z
day: '06'
department:
- _id: MaHe
doi: 10.1016/j.cmet.2019.05.010
extern: '1'
external_id:
  pmid:
  - '31178361'
intvolume: '        30'
issue: '2'
keyword:
- Cell Biology
- Molecular Biology
- Physiology
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.cmet.2019.05.010
month: '08'
oa: 1
oa_version: Published Version
page: 343-351.e3
pmid: 1
publication: Cell Metabolism
publication_identifier:
  issn:
  - 1550-4131
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Age mosaicism across multiple scales in adult tissues
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2019'
...
---
_id: '10881'
abstract:
- lang: eng
  text: Strigolactones (SLs) are a relatively recent addition to the list of plant
    hormones that control different aspects of plant development. SL signalling is
    perceived by an α/β hydrolase, DWARF 14 (D14). A close homolog of D14, KARRIKIN
    INSENSTIVE2 (KAI2), is involved in perception of an uncharacterized molecule called
    karrikin (KAR). Recent studies in Arabidopsis identified the SUPPRESSOR OF MAX2
    1 (SMAX1) and SMAX1-LIKE 7 (SMXL7) to be potential SCF–MAX2 complex-mediated proteasome
    targets of KAI2 and D14, respectively. Genetic studies on SMXL7 and SMAX1 demonstrated
    distinct developmental roles for each, but very little is known about these repressors
    in terms of their sequence features. In this study, we performed an extensive
    comparative analysis of SMXLs and determined their phylogenetic and evolutionary
    history in the plant lineage. Our results show that SMXL family members can be
    sub-divided into four distinct phylogenetic clades/classes, with an ancient SMAX1.
    Further, we identified the clade-specific motifs that have evolved and that might
    act as determinants of SL-KAR signalling specificity. These specificities resulted
    from functional diversities among the clades. Our results suggest that a gradual
    co-evolution of SMXL members with their upstream receptors D14/KAI2 provided an
    increased specificity to both the SL perception and response in land plants.
acknowledgement: "This project received funding from the European Union’s Horizon
  2020 research and innovation programme under the Marie Skłodowska-Curie Actions
  and it is co-financed by the South Moravian Region under grant agreement No. 665860
  (SS). Access to computing and storage facilities owned by parties and projects contributing
  to the national grid infrastructure, MetaCentrum, provided under the program ‘Projects
  of Large Infrastructure for Research, Development, and Innovations’ (LM2010005)
  was greatly appreciated (RSV). The project was funded by The Ministry of Education,
  Youth and Sports/MES of the Czech Republic under the project CEITEC 2020 (LQ1601)
  (TN, TRM). JF was supported by the European Research Council (project ERC-2011-StG
  20101109-PSDP) and the Czech Science Foundation GAČR (GA13-40637S). We thank Dr
  Kamel Chibani for active discussions on the evolutionary analysis and Nandan Mysore
  Vardarajan for his critical comments on the manuscript. This article reflects\r\nonly
  the authors’ views, and the EU is not responsible for any use that may be made of
  the information it contains. "
article_processing_charge: No
article_type: original
author:
- first_name: Taraka Ramji
  full_name: Moturu, Taraka Ramji
  last_name: Moturu
- first_name: Sravankumar
  full_name: Thula, Sravankumar
  last_name: Thula
- first_name: Ravi Kumar
  full_name: Singh, Ravi Kumar
  last_name: Singh
- first_name: Tomasz
  full_name: Nodzyński, Tomasz
  last_name: Nodzyński
- first_name: Radka Svobodová
  full_name: Vařeková, Radka Svobodová
  last_name: Vařeková
- first_name: Jiří
  full_name: Friml, Jiří
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
- first_name: Sibu
  full_name: Simon, Sibu
  last_name: Simon
citation:
  ama: Moturu TR, Thula S, Singh RK, et al. Molecular evolution and diversification
    of the SMXL gene family. <i>Journal of Experimental Botany</i>. 2018;69(9):2367-2378.
    doi:<a href="https://doi.org/10.1093/jxb/ery097">10.1093/jxb/ery097</a>
  apa: Moturu, T. R., Thula, S., Singh, R. K., Nodzyński, T., Vařeková, R. S., Friml,
    J., &#38; Simon, S. (2018). Molecular evolution and diversification of the SMXL
    gene family. <i>Journal of Experimental Botany</i>. Oxford University Press. <a
    href="https://doi.org/10.1093/jxb/ery097">https://doi.org/10.1093/jxb/ery097</a>
  chicago: Moturu, Taraka Ramji, Sravankumar Thula, Ravi Kumar Singh, Tomasz Nodzyński,
    Radka Svobodová Vařeková, Jiří Friml, and Sibu Simon. “Molecular Evolution and
    Diversification of the SMXL Gene Family.” <i>Journal of Experimental Botany</i>.
    Oxford University Press, 2018. <a href="https://doi.org/10.1093/jxb/ery097">https://doi.org/10.1093/jxb/ery097</a>.
  ieee: T. R. Moturu <i>et al.</i>, “Molecular evolution and diversification of the
    SMXL gene family,” <i>Journal of Experimental Botany</i>, vol. 69, no. 9. Oxford
    University Press, pp. 2367–2378, 2018.
  ista: Moturu TR, Thula S, Singh RK, Nodzyński T, Vařeková RS, Friml J, Simon S.
    2018. Molecular evolution and diversification of the SMXL gene family. Journal
    of Experimental Botany. 69(9), 2367–2378.
  mla: Moturu, Taraka Ramji, et al. “Molecular Evolution and Diversification of the
    SMXL Gene Family.” <i>Journal of Experimental Botany</i>, vol. 69, no. 9, Oxford
    University Press, 2018, pp. 2367–78, doi:<a href="https://doi.org/10.1093/jxb/ery097">10.1093/jxb/ery097</a>.
  short: T.R. Moturu, S. Thula, R.K. Singh, T. Nodzyński, R.S. Vařeková, J. Friml,
    S. Simon, Journal of Experimental Botany 69 (2018) 2367–2378.
date_created: 2022-03-18T12:43:22Z
date_published: 2018-04-13T00:00:00Z
date_updated: 2025-04-15T07:48:01Z
day: '13'
department:
- _id: JiFr
doi: 10.1093/jxb/ery097
ec_funded: 1
external_id:
  isi:
  - '000430727000016'
  pmid:
  - '29538714'
intvolume: '        69'
isi: 1
issue: '9'
keyword:
- Plant Science
- Physiology
language:
- iso: eng
month: '04'
oa_version: None
page: 2367-2378
pmid: 1
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '282300'
  name: Polarity and subcellular dynamics in plants
publication: Journal of Experimental Botany
publication_identifier:
  eissn:
  - 1460-2431
  issn:
  - 0022-0957
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular evolution and diversification of the SMXL gene family
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 69
year: '2018'
...
---
_id: '12196'
abstract:
- lang: eng
  text: SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular
    Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in
    the induction of defense responses. However, the molecular mechanisms underlying
    NLR activation and the subsequent provocation of immune responses are only partially
    characterized. To identify negative regulators of NLR-mediated immunity, a forward
    genetic screen was undertaken to search for enhancers of the dwarf, autoimmune
    gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism,
    the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display
    wild-type-like morphology and resistance. M2 progeny were screened for mutant,
    snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes.
    The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated
    expression of the pPR2-GUS defense marker reporter gene and enhanced resistance
    to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning
    and Illumina sequencing, it was determined that the muse9 mutation is in the gene
    encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10.
    The syd-10 single mutant has no observable alteration from wild-type-like resistance,
    although the syd-4 T-DNA insertion allele displays enhanced resistance to the
    bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of
    SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays
    a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated
    immunity. SYD may work with other proteins at the chromatin level to repress SNC1
    transcription; such regulation is important for fine-tuning the expression of
    NLR-encoding genes to prevent unpropitious autoimmunity.
acknowledgement: "This work was supported by the National Sciences and Engineering
  Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery
  Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the
  Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang
  and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles
  Copeland for critical reading of the manuscript."
article_processing_charge: No
article_type: original
author:
- first_name: Kaeli C.M.
  full_name: Johnson, Kaeli C.M.
  last_name: Johnson
- first_name: Shitou
  full_name: Xia, Shitou
  last_name: Xia
- first_name: Xiaoqi
  full_name: Feng, Xiaoqi
  id: e0164712-22ee-11ed-b12a-d80fcdf35958
  last_name: Feng
  orcid: 0000-0002-4008-1234
- first_name: Xin
  full_name: Li, Xin
  last_name: Li
citation:
  ama: Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively
    regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>. 2015;56(8):1616-1623.
    doi:<a href="https://doi.org/10.1093/pcp/pcv087">10.1093/pcp/pcv087</a>
  apa: Johnson, K. C. M., Xia, S., Feng, X., &#38; Li, X. (2015). The chromatin remodeler
    SPLAYED negatively regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>.
    Oxford University Press. <a href="https://doi.org/10.1093/pcp/pcv087">https://doi.org/10.1093/pcp/pcv087</a>
  chicago: Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin
    Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” <i>Plant and Cell
    Physiology</i>. Oxford University Press, 2015. <a href="https://doi.org/10.1093/pcp/pcv087">https://doi.org/10.1093/pcp/pcv087</a>.
  ieee: K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED
    negatively regulates SNC1-mediated immunity,” <i>Plant and Cell Physiology</i>,
    vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015.
  ista: Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively
    regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.
  mla: Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates
    SNC1-Mediated Immunity.” <i>Plant and Cell Physiology</i>, vol. 56, no. 8, Oxford
    University Press, 2015, pp. 1616–23, doi:<a href="https://doi.org/10.1093/pcp/pcv087">10.1093/pcp/pcv087</a>.
  short: K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015)
    1616–1623.
date_created: 2023-01-16T09:20:22Z
date_published: 2015-08-01T00:00:00Z
date_updated: 2023-05-08T11:03:23Z
department:
- _id: XiFe
doi: 10.1093/pcp/pcv087
extern: '1'
external_id:
  pmid:
  - '26063389'
intvolume: '        56'
issue: '8'
keyword:
- Cell Biology
- Plant Science
- Physiology
- General Medicine
language:
- iso: eng
month: '08'
oa_version: None
page: 1616-1623
pmid: 1
publication: Plant and Cell Physiology
publication_identifier:
  issn:
  - 0032-0781
  - 1471-9053
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2015'
...
---
_id: '12925'
abstract:
- lang: eng
  text: Normal function of organs and cells is tightly linked to the cytoarchitecture.
    Control of the cell volume is therefore vital for the organism. A widely established
    strategy of cells to counteract swelling is the activation of chloride and potassium
    channels, which leads to a net efflux of salt followed by water - a process termed
    regulatory volume decrease. Since there is evidence for swelling-dependent chloride
    channels (IClswell) being activated also during pathological processes, the identification
    of the molecular entity underlying IClswell is of utmost importance. Several proteins
    are discussed as the channel forming IClswell, i.e. phospholemman, p-glycoprotein,
    CLC-3 and ICln. In this review we would like to focus on the properties of ICln,
    a protein cloned from a Madin Darby canine kidney (MDCK) cell library whose expression
    in Xenopus laevis oocytes resulted in a nucleotide sensitive outwardly rectifying
    chloride current closely resembling the biophysical properties of IClswell.
article_processing_charge: No
article_type: original
author:
- first_name: Johannes
  full_name: Fürst, Johannes
  last_name: Fürst
- first_name: Martin
  full_name: Jakab, Martin
  last_name: Jakab
- first_name: Matthias
  full_name: König, Matthias
  last_name: König
- first_name: Markus
  full_name: Ritter, Markus
  last_name: Ritter
- first_name: Martin
  full_name: Gschwentner, Martin
  last_name: Gschwentner
- first_name: Jakob
  full_name: Rudzki, Jakob
  last_name: Rudzki
- first_name: Johann G
  full_name: Danzl, Johann G
  id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
  last_name: Danzl
  orcid: 0000-0001-8559-3973
- first_name: Michael
  full_name: Mayer, Michael
  last_name: Mayer
- first_name: Carmen M.
  full_name: Burtscher, Carmen M.
  last_name: Burtscher
- first_name: Julia
  full_name: Schirmer, Julia
  last_name: Schirmer
- first_name: Brigitte
  full_name: Maier, Brigitte
  last_name: Maier
- first_name: Manfred
  full_name: Nairz, Manfred
  last_name: Nairz
- first_name: Sabine
  full_name: Chwatal, Sabine
  last_name: Chwatal
- first_name: Markus
  full_name: Paulmichl, Markus
  last_name: Paulmichl
citation:
  ama: Fürst J, Jakab M, König M, et al. Structure and Function of the Ion Channel
    ICln. <i>Cellular Physiology and Biochemistry</i>. 2000;10(5-6):329-334. doi:<a
    href="https://doi.org/10.1159/000016374">10.1159/000016374</a>
  apa: Fürst, J., Jakab, M., König, M., Ritter, M., Gschwentner, M., Rudzki, J., …
    Paulmichl, M. (2000). Structure and Function of the Ion Channel ICln. <i>Cellular
    Physiology and Biochemistry</i>. S. Karger AG. <a href="https://doi.org/10.1159/000016374">https://doi.org/10.1159/000016374</a>
  chicago: Fürst, Johannes, Martin Jakab, Matthias König, Markus Ritter, Martin Gschwentner,
    Jakob Rudzki, Johann G Danzl, et al. “Structure and Function of the Ion Channel
    ICln.” <i>Cellular Physiology and Biochemistry</i>. S. Karger AG, 2000. <a href="https://doi.org/10.1159/000016374">https://doi.org/10.1159/000016374</a>.
  ieee: J. Fürst <i>et al.</i>, “Structure and Function of the Ion Channel ICln,”
    <i>Cellular Physiology and Biochemistry</i>, vol. 10, no. 5–6. S. Karger AG, pp.
    329–334, 2000.
  ista: Fürst J, Jakab M, König M, Ritter M, Gschwentner M, Rudzki J, Danzl JG, Mayer
    M, Burtscher CM, Schirmer J, Maier B, Nairz M, Chwatal S, Paulmichl M. 2000. Structure
    and Function of the Ion Channel ICln. Cellular Physiology and Biochemistry. 10(5–6),
    329–334.
  mla: Fürst, Johannes, et al. “Structure and Function of the Ion Channel ICln.” <i>Cellular
    Physiology and Biochemistry</i>, vol. 10, no. 5–6, S. Karger AG, 2000, pp. 329–34,
    doi:<a href="https://doi.org/10.1159/000016374">10.1159/000016374</a>.
  short: J. Fürst, M. Jakab, M. König, M. Ritter, M. Gschwentner, J. Rudzki, J.G.
    Danzl, M. Mayer, C.M. Burtscher, J. Schirmer, B. Maier, M. Nairz, S. Chwatal,
    M. Paulmichl, Cellular Physiology and Biochemistry 10 (2000) 329–334.
date_created: 2023-05-08T09:04:58Z
date_published: 2000-01-01T00:00:00Z
date_updated: 2023-05-08T10:07:10Z
doi: 10.1159/000016374
extern: '1'
external_id:
  pmid:
  - '11125213'
intvolume: '        10'
issue: 5-6
keyword:
- Physiology
language:
- iso: eng
oa_version: None
page: 329-334
pmid: 1
publication: Cellular Physiology and Biochemistry
publication_identifier:
  issn:
  - 1015-8987
  - 1421-9778
publication_status: published
publisher: S. Karger AG
quality_controlled: '1'
scopus_import: '1'
status: public
title: Structure and Function of the Ion Channel ICln
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2000'
...
