---
OA_place: publisher
OA_type: hybrid
_id: '22267'
abstract:
- lang: eng
  text: Thermal pollution, whether local or driven by global warming, threatens biodiversity
    in part through its detrimental effects on reproduction. Non-coding small RNAs
    (sRNAs) are crucial for maintaining germline developmental robustness under heat
    stress. Remarkably, we uncovered that neuronal sRNAs regulate germ cells’ thermotolerance,
    affecting both spermatogenic and oogenic germlines in a cell-non-autonomous manner.
    Furthermore, we demonstrate that, in RNAi mutants, an oxygen-sensing neural circuit,
    modulated by neuropeptide signaling, antagonizes germline maintenance, likely
    reflecting the nematode’s innate association of reduced oxygen levels with food
    availability and reproductive permissive environments. Finally, we provide evidence
    that laboratory-domesticated alleles of oxygen-response genes encoding neuropeptide
    receptor NPR-1 and hexacoordinated globin GLB-5 compromise germline thermotolerance.
    Hence, our findings raise the possibility that sensory perception, independent
    of direct environmental change, modulates germline integrity, highlighting a novel
    mechanism by which neural circuits integrate environmental information to safeguard
    reproductive fitness in fluctuating environments.
acknowledgement: We thank Itai Reiger for their assistance with experiments. We thank
  Cori Bargmann (Rockefeller University) for providing introgressed strains carrying
  HW alleles of npr-1 and glb-5. Some graphics were created with Biorender.com. We
  are grateful to WormBase for providing valuable data and resources. Some strains
  were provided by the Caenorhabditis Genetics Center (CGC), which is funded by NIH
  Office of Research Infrastructure Programs (P40 OD010440). O.R. is grateful for
  the support of the Morris Kahn Foundation. C.K.E. was supported by an EMBO fellowship
  ALTF 6-2022. This work is funded by Eric and Wendy Schmidt Fund for Strategic Innovation
  Polymath Award 0140001000 (O.R.); European Research Council grant 335624 (O.R.);
  Israel Science Foundation 979/21 (Y.B.T.); and the US-Israel Binational Science
  Foundation 2023036 (Y.B.T.).
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Chee Kiang
  full_name: Ewe, Chee Kiang
  last_name: Ewe
- first_name: Hanna
  full_name: Achache, Hanna
  last_name: Achache
- first_name: Hanna
  full_name: Schön, Hanna
  id: C8E17EDC-D7AA-11E9-B7B7-45ECE5697425
  last_name: Schön
- first_name: Leonid
  full_name: Kontorovich, Leonid
  last_name: Kontorovich
- first_name: Guy
  full_name: Teichman, Guy
  last_name: Teichman
- first_name: Shir
  full_name: Weiss, Shir
  last_name: Weiss
- first_name: Anna
  full_name: Mogilevskaya, Anna
  last_name: Mogilevskaya
- first_name: Myriam
  full_name: Valenski, Myriam
  last_name: Valenski
- first_name: Sarit
  full_name: Anava, Sarit
  last_name: Anava
- first_name: Rutwik
  full_name: Bardapurkar, Rutwik
  last_name: Bardapurkar
- first_name: Hila
  full_name: Gingold, Hila
  last_name: Gingold
- first_name: Rachel
  full_name: Posner, Rachel
  last_name: Posner
- first_name: Olga
  full_name: Antonova, Olga
  last_name: Antonova
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
- first_name: Yonatan B.
  full_name: Tzur, Yonatan B.
  last_name: Tzur
- first_name: Oded
  full_name: Rechavi, Oded
  last_name: Rechavi
citation:
  ama: Ewe CK, Achache H, Schön H, et al. Neuronal RNAi and oxygen-sensing circuit
    shape germline resilience to heat stress. <i>Current Biology</i>. doi:<a href="https://doi.org/10.1016/j.cub.2026.06.016">10.1016/j.cub.2026.06.016</a>
  apa: Ewe, C. K., Achache, H., Schön, H., Kontorovich, L., Teichman, G., Weiss, S.,
    … Rechavi, O. (n.d.). Neuronal RNAi and oxygen-sensing circuit shape germline
    resilience to heat stress. <i>Current Biology</i>. Elsevier. <a href="https://doi.org/10.1016/j.cub.2026.06.016">https://doi.org/10.1016/j.cub.2026.06.016</a>
  chicago: Ewe, Chee Kiang, Hanna Achache, Hanna Schön, Leonid Kontorovich, Guy Teichman,
    Shir Weiss, Anna Mogilevskaya, et al. “Neuronal RNAi and Oxygen-Sensing Circuit
    Shape Germline Resilience to Heat Stress.” <i>Current Biology</i>. Elsevier, n.d.
    <a href="https://doi.org/10.1016/j.cub.2026.06.016">https://doi.org/10.1016/j.cub.2026.06.016</a>.
  ieee: C. K. Ewe <i>et al.</i>, “Neuronal RNAi and oxygen-sensing circuit shape germline
    resilience to heat stress,” <i>Current Biology</i>. Elsevier.
  ista: Ewe CK, Achache H, Schön H, Kontorovich L, Teichman G, Weiss S, Mogilevskaya
    A, Valenski M, Anava S, Bardapurkar R, Gingold H, Posner R, Antonova O, de Bono
    M, Tzur YB, Rechavi O. Neuronal RNAi and oxygen-sensing circuit shape germline
    resilience to heat stress. Current Biology.
  mla: Ewe, Chee Kiang, et al. “Neuronal RNAi and Oxygen-Sensing Circuit Shape Germline
    Resilience to Heat Stress.” <i>Current Biology</i>, Elsevier, doi:<a href="https://doi.org/10.1016/j.cub.2026.06.016">10.1016/j.cub.2026.06.016</a>.
  short: C.K. Ewe, H. Achache, H. Schön, L. Kontorovich, G. Teichman, S. Weiss, A.
    Mogilevskaya, M. Valenski, S. Anava, R. Bardapurkar, H. Gingold, R. Posner, O.
    Antonova, M. de Bono, Y.B. Tzur, O. Rechavi, Current Biology (n.d.).
das_tickbox: '1'
dataavailabilitystatement: "* All NGS data are available through GEO under accession
  number GSE331410.\r\n* This paper does not report original code.\r\n* Any additional
  information required to reanalyze the data reported in this paper is available from
  the lead contact upon request."
date_created: 2026-07-12T22:02:18Z
date_published: 2026-07-06T00:00:00Z
date_updated: 2026-07-13T08:23:09Z
day: '06'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1016/j.cub.2026.06.016
external_id:
  pmid:
  - '42409014'
has_accepted_license: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.cub.2026.06.016
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Current Biology
publication_identifier:
  eissn:
  - 1879-0445
  issn:
  - 0960-9822
publication_status: inpress
publisher: Elsevier
quality_controlled: '1'
researchdata_availability: upon request
scopus_import: '1'
status: public
supplementarymaterial: yes
title: Neuronal RNAi and oxygen-sensing circuit shape germline resilience to heat
  stress
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
year: '2026'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '22306'
abstract:
- lang: eng
  text: "The AP3 complex mediates cargo sorting and carrier assembly for the trafficking
    of transmembrane proteins from endosomes to lysosomes. AP3 is generally believed
    to localize to clathrin-free, ARF1-positive, elongated carriers in cells, but
    the architecture of AP3-based coats was unknown. Using in vitro reconstitution
    and cryo–electron tomography, we demonstrate that AP3:ARF1 spontaneously remodels
    membranes containing cargo and the phosphoinositide PI(3,5)P\r\n                    <jats:sub>2</jats:sub>\r\n
    \                   into tubular structures coated in spiraling rows of AP3 arches
    and ARF1 dimers. Targeted point mutations disrupting critical AP3:ARF1 and AP3:AP3
    lattice interfaces disrupt AP3 recruitment, carrier formation, and lysosomal cargo
    trafficking in cells. We propose that AP3 generates tubular carriers on endosomes
    by organizing ARF1 dimers into elongated membrane-deforming arrays while simultaneously
    selecting cargo. By demonstrating that AP3:ARF1 can generate carriers without
    using a clathrin lattice, we explain the clathrin independence of AP3-mediated
    trafficking."
acknowledgement: "We thank P. Luzio, N. Bright, and M. S. Robinson for helpful discussions;\r\nJ.
  Stacey and Y. Fujiharu for technical discussions and assistance; F. Beck for assistance
  with\r\ncomputing infrastructure; and M. Riggi for discussion of data presentation
  and figure design.\r\nCryo-E\r\nM data was collected at the Department of Cell and
  Virus Structure, Max Planck Institute\r\nof Biochemistry. Funding: This work was
  funded by: the Wellcome Trust, Wellcome Discovery\r\nAward 227915/Z/23/Z (to D.J.O.,
  J.A.G.B., and D.G.S.) and Wellcome PRF 207455/Z/17/Z (to\r\nD.J.O.); the Max Planck
  Society (to J.A.G.B.); the Medical Research Council (UKRI) MC_\r\nUP_1201/16 (to
  J.A.G.B.) and MRC DT P MR/N013433/1 (to J.G.G.K.); EMBO Long-term\r\nPostdoctoral
  Fellowship ALT F-383-\r\n2022\r\n(to G.T.); and the Wellcome Trust/Royal Society,
  Sir\r\nHenry Dale Fellowship 210481 (to D.C.G) and the Biotechnology and Biological
  Sciences\r\nResearch Council (UKRI) responsive mode grants BB/W005905/1 and UKRI715
  (to D.C.G.)."
article_number: eaed1529
article_processing_charge: Yes
article_type: original
author:
- first_name: Jonathan G.G.
  full_name: Kaufman, Jonathan G.G.
  last_name: Kaufman
- first_name: Grigory
  full_name: Tagiltsev, Grigory
  last_name: Tagiltsev
- first_name: Danièle S.
  full_name: Stalder, Danièle S.
  last_name: Stalder
- first_name: Rebecca J.
  full_name: Taylor, Rebecca J.
  last_name: Taylor
- first_name: Ioana
  full_name: Sava, Ioana
  last_name: Sava
- first_name: Hui
  full_name: Guo, Hui
  last_name: Guo
- first_name: Katarzyna A.
  full_name: Ciazynska, Katarzyna A.
  last_name: Ciazynska
- first_name: Nathan R.
  full_name: Zaccai, Nathan R.
  last_name: Zaccai
- first_name: Sally R.
  full_name: Gray, Sally R.
  last_name: Gray
- first_name: Yvonne
  full_name: Vallis, Yvonne
  id: 05A2795C-31B5-11EA-83A7-7DA23DDC885E
  last_name: Vallis
  orcid: 0000-0002-5408-5906
- first_name: Stefan
  full_name: Höning, Stefan
  last_name: Höning
- first_name: Bernard T.
  full_name: Kelly, Bernard T.
  last_name: Kelly
- first_name: David C.
  full_name: Gershlick, David C.
  last_name: Gershlick
- first_name: John A.G.
  full_name: Briggs, John A.G.
  last_name: Briggs
- first_name: David J.
  full_name: Owen, David J.
  last_name: Owen
citation:
  ama: Kaufman JGG, Tagiltsev G, Stalder DS, et al. Architecture of clathrin-independent
    AP3:ARF1-coated carriers. <i>Science Advances</i>. 2026;12(20). doi:<a href="https://doi.org/10.1126/sciadv.aed1529">10.1126/sciadv.aed1529</a>
  apa: Kaufman, J. G. G., Tagiltsev, G., Stalder, D. S., Taylor, R. J., Sava, I.,
    Guo, H., … Owen, D. J. (2026). Architecture of clathrin-independent AP3:ARF1-coated
    carriers. <i>Science Advances</i>. American Association for the Advancement of
    Science. <a href="https://doi.org/10.1126/sciadv.aed1529">https://doi.org/10.1126/sciadv.aed1529</a>
  chicago: Kaufman, Jonathan G.G., Grigory Tagiltsev, Danièle S. Stalder, Rebecca
    J. Taylor, Ioana Sava, Hui Guo, Katarzyna A. Ciazynska, et al. “Architecture of
    Clathrin-Independent AP3:ARF1-Coated Carriers.” <i>Science Advances</i>. American
    Association for the Advancement of Science, 2026. <a href="https://doi.org/10.1126/sciadv.aed1529">https://doi.org/10.1126/sciadv.aed1529</a>.
  ieee: J. G. G. Kaufman <i>et al.</i>, “Architecture of clathrin-independent AP3:ARF1-coated
    carriers,” <i>Science Advances</i>, vol. 12, no. 20. American Association for
    the Advancement of Science, 2026.
  ista: Kaufman JGG, Tagiltsev G, Stalder DS, Taylor RJ, Sava I, Guo H, Ciazynska
    KA, Zaccai NR, Gray SR, Vallis Y, Höning S, Kelly BT, Gershlick DC, Briggs JAG,
    Owen DJ. 2026. Architecture of clathrin-independent AP3:ARF1-coated carriers.
    Science Advances. 12(20), eaed1529.
  mla: Kaufman, Jonathan G. G., et al. “Architecture of Clathrin-Independent AP3:ARF1-Coated
    Carriers.” <i>Science Advances</i>, vol. 12, no. 20, eaed1529, American Association
    for the Advancement of Science, 2026, doi:<a href="https://doi.org/10.1126/sciadv.aed1529">10.1126/sciadv.aed1529</a>.
  short: J.G.G. Kaufman, G. Tagiltsev, D.S. Stalder, R.J. Taylor, I. Sava, H. Guo,
    K.A. Ciazynska, N.R. Zaccai, S.R. Gray, Y. Vallis, S. Höning, B.T. Kelly, D.C.
    Gershlick, J.A.G. Briggs, D.J. Owen, Science Advances 12 (2026).
das_tickbox: '1'
dataavailabilitystatement: "Structures determined by electron microscopy are deposited
  in the Electron\r\nMicroscopy Data Bank under accession codes EMD-54255,\r\nEMD-54256,\r\nEMD-54257,\r\nand\r\nEMD-54258.\r\nCorresponding
  molecular models are deposited in the Protein Data Bank under\r\naccession codes
  9RTW, 9RTX, 9RTY, and 9RTZ. All additional data and code required to\r\nevaluate
  and reproduce the results in the paper are present in the paper and/or the\r\nsupplementary
  materials. Any code used is explicitly stated and available in the original\r\npublications.
  Plasmids and cell lines can be requested by writing to D.C.G. (dg553@ cam. ac. uk)\r\nor
  D.J.O. (djo30@ cam. ac. uk). All reasonable requests for materials will be honored."
date_created: 2026-07-13T10:52:15Z
date_published: 2026-05-15T00:00:00Z
date_updated: 2026-07-14T06:52:00Z
day: '15'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1126/sciadv.aed1529
file:
- access_level: open_access
  checksum: 461b5f73941fe6b5df2a129c7563601f
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  creator: dernst
  date_created: 2026-07-14T06:45:37Z
  date_updated: 2026-07-14T06:45:37Z
  file_id: '22331'
  file_name: 2026_ScienceAdv_Kaufman.pdf
  file_size: 8269526
  relation: main_file
  success: 1
file_date_updated: 2026-07-14T06:45:37Z
has_accepted_license: '1'
intvolume: '        12'
issue: '20'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: Science Advances
publication_identifier:
  eissn:
  - 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
researchdata_availability: yes
scopus_import: '1'
status: public
supplementarymaterial: yes
title: Architecture of clathrin-independent AP3:ARF1-coated carriers
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2026'
...
---
APC_amount: 7068 EUR
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '20929'
abstract:
- lang: eng
  text: Insulin/insulin-like growth factor signaling inhibits FOXO transcription factors
    to control development, homeostasis, and aging. Here, we use proximity labeling
    to identify proteins interacting with the C. elegans FOXO DAF-16. We show that
    in well-fed, unstressed animals harboring active insulin signaling, DAF-16 forms
    a complex with the PAR-1/MARK serine/threonine kinase, a key regulator of cell
    polarity. PAR-1 inhibits DAF-16 accumulation and promotes DAF-16 phosphorylation
    at S249, at a conserved motif that PAR-1/human MARK2 phosphorylates in vitro.
    DAF-2 insulin-like receptor signaling stimulates DAF-16 S249 phosphorylation,
    suggesting DAF-2 activates PAR-1. DAF-2 also promotes PAR-1 expression by inhibiting
    DAF-16. PAR-1 knockdown, or DAF-16 S249A, prolong lifespan, whereas phosphomimetic
    DAF-16 S249D suppresses the longevity of daf-2 mutants. At low insulin signaling,
    DAF-16 proximity labeling highlights transcription factors, chromatin regulators,
    and DNA repair proteins. One interactor, the zinc finger/homeobox protein ZFH-2/ZFHX3,
    forms a complex with DAF-16 and prolongs lifespan. Our work provides entry points
    for hypothesis-driven studies of FOXO function and longevity.
acknowledged_ssus:
- _id: Bio
acknowledgement: We thank de Bono lab members for helpful comments on the manuscript,
  and the Mass Spec Facility at the Max Perutz Labs, notably WeiQiang Chen and Markus
  Hartl, for invaluable discussions and comments on mass spec analyses of worm samples.
  All LC-MS/MS analyses were performed on instruments of the Vienna BioCenter Core
  Facilities (VBCF). Microscopy was supported by the Scientific Services Units (SSU)
  of ISTA through resources provided by the Imaging & Optics Facility (IOF). We are
  grateful to Dr. Geraldine Seydoux (Johns Hopkins University) for worm strains and
  plasmids, and Dr. Seung-Jae V. Lee (KAIST) for RNAi clones. We are grateful to Ekaterina
  Lashmanova for designing the daf-16::TbID::mNG::3xFLAG knock-in construct and for
  her outstanding support in the lab. This work was supported by a Wellcome Investigator
  Award (209504/A/17/Z) to MdB and an ISTplus Fellowship to MA (Marie Sklodowska-Curie
  agreement No 754411).
article_number: '11355'
article_processing_charge: Yes
article_type: original
author:
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Hanna
  full_name: Schön, Hanna
  id: C8E17EDC-D7AA-11E9-B7B7-45ECE5697425
  last_name: Schön
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Artan M, Schön H, de Bono M. Proximity labeling of DAF-16 FOXO highlights aging
    regulatory proteins. <i>Nature Communications</i>. 2025;16. doi:<a href="https://doi.org/10.1038/s41467-025-66409-0">10.1038/s41467-025-66409-0</a>
  apa: Artan, M., Schön, H., &#38; de Bono, M. (2025). Proximity labeling of DAF-16
    FOXO highlights aging regulatory proteins. <i>Nature Communications</i>. Springer
    Nature. <a href="https://doi.org/10.1038/s41467-025-66409-0">https://doi.org/10.1038/s41467-025-66409-0</a>
  chicago: Artan, Murat, Hanna Schön, and Mario de Bono. “Proximity Labeling of DAF-16
    FOXO Highlights Aging Regulatory Proteins.” <i>Nature Communications</i>. Springer
    Nature, 2025. <a href="https://doi.org/10.1038/s41467-025-66409-0">https://doi.org/10.1038/s41467-025-66409-0</a>.
  ieee: M. Artan, H. Schön, and M. de Bono, “Proximity labeling of DAF-16 FOXO highlights
    aging regulatory proteins,” <i>Nature Communications</i>, vol. 16. Springer Nature,
    2025.
  ista: Artan M, Schön H, de Bono M. 2025. Proximity labeling of DAF-16 FOXO highlights
    aging regulatory proteins. Nature Communications. 16, 11355.
  mla: Artan, Murat, et al. “Proximity Labeling of DAF-16 FOXO Highlights Aging Regulatory
    Proteins.” <i>Nature Communications</i>, vol. 16, 11355, Springer Nature, 2025,
    doi:<a href="https://doi.org/10.1038/s41467-025-66409-0">10.1038/s41467-025-66409-0</a>.
  short: M. Artan, H. Schön, M. de Bono, Nature Communications 16 (2025).
corr_author: '1'
date_created: 2026-01-04T23:01:34Z
date_published: 2025-12-11T00:00:00Z
date_updated: 2026-05-20T08:10:18Z
day: '11'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1038/s41467-025-66409-0
ec_funded: 1
external_id:
  pmid:
  - '41381452'
file:
- access_level: open_access
  checksum: 748e2e003b878b85b6048d51621d6aae
  content_type: application/pdf
  creator: dernst
  date_created: 2026-01-05T10:58:28Z
  date_updated: 2026-01-05T10:58:28Z
  file_id: '20941'
  file_name: 2025_NatureComm_Artan.pdf
  file_size: 1642352
  relation: main_file
  success: 1
file_date_updated: 2026-01-05T10:58:28Z
has_accepted_license: '1'
intvolume: '        16'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Proximity labeling of DAF-16 FOXO highlights aging regulatory proteins
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: 16
year: '2025'
...
---
OA_place: publisher
OA_type: hybrid
_id: '15016'
abstract:
- lang: eng
  text: Amphibians, by virtue of their phylogenetic position, provide invaluable insights
    on nervous system evolution, development, and remodeling. The genetic toolkit
    for amphibians, however, remains limited. Recombinant adeno-associated viral vectors
    (AAVs) are a powerful alternative to transgenesis for labeling and manipulating
    neurons. Although successful in mammals, AAVs have never been shown to transduce
    amphibian cells efficiently. We screened AAVs in three amphibian species—the frogs
    Xenopus laevis and Pelophylax bedriagae and the salamander Pleurodeles waltl—and
    identified at least two AAV serotypes per species that transduce neurons. In developing
    amphibians, AAVs labeled groups of neurons generated at the same time during development.
    In the mature brain, AAVrg retrogradely traced long-range projections. Our study
    introduces AAVs as a tool for amphibian research, establishes a generalizable
    workflow for AAV screening in new species, and expands opportunities for cross-species
    comparisons of nervous system development, function, and evolution.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
acknowledgement: 'We thank members of the Sweeney, Tosches, Shein-Idelson, Yamaguchi,
  Kelley, and Cline Labs for their contributions to this project, discussion, and
  support. We additionally thank the Beckman Institute CLOVER Center and Viviana Gradinaru
  (Caltech), Kimberly Ritola (UNC NeuroTools), and Flavia Gomez-Leite (ISTA Viral
  Core) for AAV production and consultation; Andras Simon and Alberto Joven (Karolinska
  Institute) for feedback; Elizabeth Bagnato-Cohen (Columbia) for project coordination;
  our animal care and imaging facilities; the amphibian stock centers (NXR, EXRC,
  and XenopusExpress); and our funding sources: NSF IOS 2110086 (D.B.K., L.B.S., M.A.T.,
  A.Y., and H.T.C.); US-Israel Binational Science Foundation (BSF) 2020702 (M.S.-I.);
  FTI Strategy Lower Austria Dissertation FT121-D-046 (D.V.); Horizon Europe ERC Starting
  Grant 101041551 and Special Research Programme (SFB) of the Austrian Science Fund
  (FWF) project F7814-B (L.B.S.); NIH grant R35GM146973, Rita Allen Foundation Award
  GA_032522_FE, and CZI Ben Barres Early Career Acceleration Award 2023-331758 (M.A.T.);
  EMBO Long-Term Fellowship ALTF 874-2021 (A.D.); and NSF GRFP DGE 2036197 (E.C.B.J.).'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Eliza C.B.
  full_name: Jaeger, Eliza C.B.
  last_name: Jaeger
- first_name: David
  full_name: Vijatovic, David
  id: cf391e77-ec3c-11ea-a124-d69323410b58
  last_name: Vijatovic
- first_name: Astrid
  full_name: Deryckere, Astrid
  last_name: Deryckere
- first_name: Nikol
  full_name: Zorin, Nikol
  last_name: Zorin
- first_name: Akemi L.
  full_name: Nguyen, Akemi L.
  last_name: Nguyen
- first_name: Georgiy
  full_name: Ivanian, Georgiy
  id: eaf2b366-cfd1-11ee-bbdf-c8790f800a05
  last_name: Ivanian
- first_name: Jamie
  full_name: Woych, Jamie
  last_name: Woych
- first_name: Rebecca C
  full_name: Arnold, Rebecca C
  id: d6cce458-14c9-11ed-a755-c1c8fc6fde6f
  last_name: Arnold
- first_name: Alonso
  full_name: Ortega Gurrola, Alonso
  last_name: Ortega Gurrola
- first_name: Arik
  full_name: Shvartsman, Arik
  last_name: Shvartsman
- first_name: Francesca
  full_name: Barbieri, Francesca
  id: a9492887-8972-11ed-ae7b-bfae10998254
  last_name: Barbieri
- first_name: Florina-Alexandra
  full_name: Toma, Florina-Alexandra
  id: 85dd99f2-15b2-11ec-abd3-d1ae4d57f3b5
  last_name: Toma
- first_name: Gary J.
  full_name: Gorbsky, Gary J.
  last_name: Gorbsky
- first_name: Marko E.
  full_name: Horb, Marko E.
  last_name: Horb
- first_name: Hollis T.
  full_name: Cline, Hollis T.
  last_name: Cline
- first_name: Timothy F.
  full_name: Shay, Timothy F.
  last_name: Shay
- first_name: Darcy B.
  full_name: Kelley, Darcy B.
  last_name: Kelley
- first_name: Ayako
  full_name: Yamaguchi, Ayako
  last_name: Yamaguchi
- first_name: Mark
  full_name: Shein-Idelson, Mark
  last_name: Shein-Idelson
- first_name: Maria Antonietta
  full_name: Tosches, Maria Antonietta
  last_name: Tosches
- first_name: Lora Beatrice Jaeger
  full_name: Sweeney, Lora Beatrice Jaeger
  id: 56BE8254-C4F0-11E9-8E45-0B23E6697425
  last_name: Sweeney
  orcid: 0000-0001-9242-5601
citation:
  ama: Jaeger ECB, Vijatovic D, Deryckere A, et al. Adeno-associated viral tools to
    trace neural development and connectivity across amphibians. <i>Developmental
    Cell</i>. 2025;60(5):794-812.e6. doi:<a href="https://doi.org/10.1016/j.devcel.2024.10.025">10.1016/j.devcel.2024.10.025</a>
  apa: Jaeger, E. C. B., Vijatovic, D., Deryckere, A., Zorin, N., Nguyen, A. L., Ivanian,
    G., … Sweeney, L. B. (2025). Adeno-associated viral tools to trace neural development
    and connectivity across amphibians. <i>Developmental Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.devcel.2024.10.025">https://doi.org/10.1016/j.devcel.2024.10.025</a>
  chicago: Jaeger, Eliza C.B., David Vijatovic, Astrid Deryckere, Nikol Zorin, Akemi
    L. Nguyen, Georgiy Ivanian, Jamie Woych, et al. “Adeno-Associated Viral Tools
    to Trace Neural Development and Connectivity across Amphibians.” <i>Developmental
    Cell</i>. Elsevier, 2025. <a href="https://doi.org/10.1016/j.devcel.2024.10.025">https://doi.org/10.1016/j.devcel.2024.10.025</a>.
  ieee: E. C. B. Jaeger <i>et al.</i>, “Adeno-associated viral tools to trace neural
    development and connectivity across amphibians,” <i>Developmental Cell</i>, vol.
    60, no. 5. Elsevier, p. 794–812.e6, 2025.
  ista: Jaeger ECB, Vijatovic D, Deryckere A, Zorin N, Nguyen AL, Ivanian G, Woych
    J, Arnold RC, Ortega Gurrola A, Shvartsman A, Barbieri F, Toma F-A, Gorbsky GJ,
    Horb ME, Cline HT, Shay TF, Kelley DB, Yamaguchi A, Shein-Idelson M, Tosches MA,
    Sweeney LB. 2025. Adeno-associated viral tools to trace neural development and
    connectivity across amphibians. Developmental Cell. 60(5), 794–812.e6.
  mla: Jaeger, Eliza C. B., et al. “Adeno-Associated Viral Tools to Trace Neural Development
    and Connectivity across Amphibians.” <i>Developmental Cell</i>, vol. 60, no. 5,
    Elsevier, 2025, p. 794–812.e6, doi:<a href="https://doi.org/10.1016/j.devcel.2024.10.025">10.1016/j.devcel.2024.10.025</a>.
  short: E.C.B. Jaeger, D. Vijatovic, A. Deryckere, N. Zorin, A.L. Nguyen, G. Ivanian,
    J. Woych, R.C. Arnold, A. Ortega Gurrola, A. Shvartsman, F. Barbieri, F.-A. Toma,
    G.J. Gorbsky, M.E. Horb, H.T. Cline, T.F. Shay, D.B. Kelley, A. Yamaguchi, M.
    Shein-Idelson, M.A. Tosches, L.B. Sweeney, Developmental Cell 60 (2025) 794–812.e6.
corr_author: '1'
date_created: 2024-02-20T09:20:32Z
date_published: 2025-03-10T00:00:00Z
date_updated: 2025-09-30T10:00:55Z
day: '10'
ddc:
- '570'
department:
- _id: LoSw
- _id: MaDe
- _id: GaNo
doi: 10.1016/j.devcel.2024.10.025
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oa_version: Published Version
page: 794-812.e6
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project:
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  grant_number: FTI21-D-046
  name: Development of V1 interneuron diversity during swim-to-walk transition of
    Xenopus metamorphosis
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    transition: cell type to connection diversity'
publication: Developmental Cell
publication_identifier:
  eissn:
  - 1878-1551
  issn:
  - 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Adeno-associated viral tools to trace neural development and connectivity across
  amphibians
tmp:
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type: journal_article
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...
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acknowledgement: "This work was supported by EMBO (ALTF 302-2019 to Niko Amin-Wetzel),
  the FWF\r\n(ESPRIT PR1054E140 to Niko Amin-Wetzel), the European Research Council\r\n(Advanced
  Grant 269058 to Mario de Bono) and Wellcome (209504/A/17/Z\r\nInvestigator Award
  to Mario de Bono). "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Hanna
  full_name: Schön, Hanna
  id: C8E17EDC-D7AA-11E9-B7B7-45ECE5697425
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citation:
  ama: Schön H. The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
    GPCRs. 2025. doi:<a href="https://doi.org/10.15479/AT-ISTA-20167">10.15479/AT-ISTA-20167</a>
  apa: Schön, H. (2025). <i>The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs
    encoding GPCRs</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT-ISTA-20167">https://doi.org/10.15479/AT-ISTA-20167</a>
  chicago: Schön, Hanna. “The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs
    Encoding GPCRs.” Institute of Science and Technology Austria, 2025. <a href="https://doi.org/10.15479/AT-ISTA-20167">https://doi.org/10.15479/AT-ISTA-20167</a>.
  ieee: H. Schön, “The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
    GPCRs,” Institute of Science and Technology Austria, 2025.
  ista: Schön H. 2025. The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
    GPCRs. Institute of Science and Technology Austria.
  mla: Schön, Hanna. <i>The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs Encoding
    GPCRs</i>. Institute of Science and Technology Austria, 2025, doi:<a href="https://doi.org/10.15479/AT-ISTA-20167">10.15479/AT-ISTA-20167</a>.
  short: H. Schön, The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs Encoding
    GPCRs, Institute of Science and Technology Austria, 2025.
corr_author: '1'
date_created: 2025-08-13T11:13:13Z
date_published: 2025-08-13T00:00:00Z
date_updated: 2026-04-07T11:50:26Z
day: '13'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
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doi: 10.15479/AT-ISTA-20167
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  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
- _id: 23813290-32DE-11EA-91FC-C7463DDC885E
  grant_number: ALTF 302-2019
  name: Control of gene expression at the endoplasmic reticulum
publication_identifier:
  isbn:
  - 978-3-99078-061-9
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
status: public
supervisor:
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
title: The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding GPCRs
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
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  short: CC BY (4.0)
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2025'
...
---
OA_place: publisher
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acknowledged_ssus:
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- _id: Bio
acknowledgement: "I would also like to acknowledge the funding that I received from
  the European Union’s\r\nHorizon 2020 research and Innovation programme under the
  Marie Sklodowska-Curie\r\nGrant Agreement No. 665385. This work would not have been
  possible without the contribution and support of people\r\nbehind the scientific
  service units at ISTA: the Life Science Facility (LSF), Imaging and\r\nOptics Facility
  (IOF), the Bioinformatics Unit, Protein Services Unit and\r\nElectrophysiology Unit.
  I would also like to recognize the work of people at the Vienna\r\nBiocenter (VBC)
  Mass Spectrometry Facility, particularly Markus Hartl and WeiQiang\r\nChen. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Michaela
  full_name: Misova, Michaela
  id: 495A3C32-F248-11E8-B48F-1D18A9856A87
  last_name: Misova
  orcid: 0000-0003-2427-6856
citation:
  ama: Misova M. Dissecting gap junction biology using the C. elegans nervous system.
    2025. doi:<a href="https://doi.org/10.15479/AT-ISTA-20485">10.15479/AT-ISTA-20485</a>
  apa: Misova, M. (2025). <i>Dissecting gap junction biology using the C. elegans
    nervous system</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT-ISTA-20485">https://doi.org/10.15479/AT-ISTA-20485</a>
  chicago: Misova, Michaela. “Dissecting Gap Junction Biology Using the C. Elegans
    Nervous System.” Institute of Science and Technology Austria, 2025. <a href="https://doi.org/10.15479/AT-ISTA-20485">https://doi.org/10.15479/AT-ISTA-20485</a>.
  ieee: M. Misova, “Dissecting gap junction biology using the C. elegans nervous system,”
    Institute of Science and Technology Austria, 2025.
  ista: Misova M. 2025. Dissecting gap junction biology using the C. elegans nervous
    system. Institute of Science and Technology Austria.
  mla: Misova, Michaela. <i>Dissecting Gap Junction Biology Using the C. Elegans Nervous
    System</i>. Institute of Science and Technology Austria, 2025, doi:<a href="https://doi.org/10.15479/AT-ISTA-20485">10.15479/AT-ISTA-20485</a>.
  short: M. Misova, Dissecting Gap Junction Biology Using the C. Elegans Nervous System,
    Institute of Science and Technology Austria, 2025.
corr_author: '1'
date_created: 2025-10-17T16:15:09Z
date_published: 2025-10-23T00:00:00Z
date_updated: 2026-04-07T11:54:00Z
day: '23'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: MaDe
doi: 10.15479/AT-ISTA-20485
ec_funded: 1
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language:
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month: '10'
oa_version: Published Version
page: '155'
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
publication_identifier:
  isbn:
  - 978-3-99078-068-8
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
status: public
supervisor:
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
title: Dissecting gap junction biology using the C. elegans nervous system
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2025'
...
---
OA_place: publisher
OA_type: hybrid
_id: '19498'
abstract:
- lang: eng
  text: A dynamic interplay between fast synaptic signals and slower neuromodulatory
    signals controls the excitatory/inhibitory (E/I) balance within neuronal circuits.
    The mechanisms by which neuropeptide signaling is regulated to maintain E/I balance
    remain uncertain. We designed a genetic screen to isolate genes involved in the
    peptidergic maintenance of the E/I balance in the C. elegans motor circuit. This
    screen identified the C. elegans orthologs of the presynaptic phosphoprotein synapsin
    (snn-1) and the protein phosphatase 1 (PP1) regulatory subunit PHACTR1 (phac-1).
    We demonstrate that both phac-1 and snn-1 alter the motor behavior of C. elegans,
    and genetic interactions suggest that SNN-1 contributes to PP1-PHAC-1 holoenzyme
    signaling. De novo variants of human PHACTR1, associated with early-onset epilepsies
    [developmental and epileptic encephalopathy 70 (DEE70)], when expressed in C.
    elegans resulted in constitutive PP1-PHAC-1 holoenzyme activity. Unregulated PP1-PHAC-1
    signaling alters the synapsin and actin cytoskeleton and increases neuropeptide
    release by cholinergic motor neurons, which secondarily affects the presynaptic
    vesicle cycle. Together, these results clarify the dominant mechanisms of action
    of the DEE70 alleles and suggest that altered neuropeptide release may alter E/I
    balance in DEE70.
acknowledgement: P.L. is a research associate of the Belgian National Fund for Scientific
  Research (FRS-FNRS). K.S., M.S.-G., S.S., and P.L. are supported by grants from
  the FRS-FNRS. This work was supported by an Advanced ERC Grant (269058 ACMO) to
  M.D.B. We thank the team of Alexander Gottschalk for the snn-1(S9A) strain. We thank
  the Imaging Facility of the Faculty of Medicine (LiMiF) of the Universite Libre
  de Bruxelles, supported by FRS-FNRS. This work made use of instruments in the Electron
  Microscopy Core of the University of Illinois Chicago Research Resources Center
  as well as the BioCryo facility of Northwestern University's NUANCE Center, which
  has received support from the SHyNE Resource (NSF ECCS-2025633), the IIN, and Northwestern's
  MRSEC program (NSF DMR-2308691). Some strains were provided by the CGC, which is
  funded by NIH Office of Research Infrastructure Programs (P40 OD010440).
article_number: e1767232024
article_processing_charge: No
article_type: original
author:
- first_name: Aikaterini
  full_name: Stratigi, Aikaterini
  last_name: Stratigi
- first_name: Miguel
  full_name: Soler-García, Miguel
  last_name: Soler-García
- first_name: Mia
  full_name: Krout, Mia
  last_name: Krout
- first_name: Shikha
  full_name: Shukla, Shikha
  last_name: Shukla
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
- first_name: Janet E.
  full_name: Richmond, Janet E.
  last_name: Richmond
- first_name: Patrick
  full_name: Laurent, Patrick
  last_name: Laurent
citation:
  ama: Stratigi A, Soler-García M, Krout M, et al. Neuroendocrine control of synaptic
    transmission by PHAC-1 in C. elegans. <i>Journal of Neuroscience</i>. 2025;45(13).
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">10.1523/JNEUROSCI.1767-23.2024</a>
  apa: Stratigi, A., Soler-García, M., Krout, M., Shukla, S., de Bono, M., Richmond,
    J. E., &#38; Laurent, P. (2025). Neuroendocrine control of synaptic transmission
    by PHAC-1 in C. elegans. <i>Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">https://doi.org/10.1523/JNEUROSCI.1767-23.2024</a>
  chicago: Stratigi, Aikaterini, Miguel Soler-García, Mia Krout, Shikha Shukla, Mario
    de Bono, Janet E. Richmond, and Patrick Laurent. “Neuroendocrine Control of Synaptic
    Transmission by PHAC-1 in C. Elegans.” <i>Journal of Neuroscience</i>. Society
    for Neuroscience, 2025. <a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">https://doi.org/10.1523/JNEUROSCI.1767-23.2024</a>.
  ieee: A. Stratigi <i>et al.</i>, “Neuroendocrine control of synaptic transmission
    by PHAC-1 in C. elegans,” <i>Journal of Neuroscience</i>, vol. 45, no. 13. Society
    for Neuroscience, 2025.
  ista: Stratigi A, Soler-García M, Krout M, Shukla S, de Bono M, Richmond JE, Laurent
    P. 2025. Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans.
    Journal of Neuroscience. 45(13), e1767232024.
  mla: Stratigi, Aikaterini, et al. “Neuroendocrine Control of Synaptic Transmission
    by PHAC-1 in C. Elegans.” <i>Journal of Neuroscience</i>, vol. 45, no. 13, e1767232024,
    Society for Neuroscience, 2025, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">10.1523/JNEUROSCI.1767-23.2024</a>.
  short: A. Stratigi, M. Soler-García, M. Krout, S. Shukla, M. de Bono, J.E. Richmond,
    P. Laurent, Journal of Neuroscience 45 (2025).
date_created: 2025-04-06T22:01:32Z
date_published: 2025-03-26T00:00:00Z
date_updated: 2025-09-30T11:29:28Z
day: '26'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1523/JNEUROSCI.1767-23.2024
external_id:
  isi:
  - '001460952700001'
  pmid:
  - '39919830'
file:
- access_level: open_access
  checksum: 7befc0168f4cd5bd2b0fcff9e2a94784
  content_type: application/pdf
  creator: dernst
  date_created: 2025-04-07T11:57:19Z
  date_updated: 2025-09-27T22:30:02Z
  embargo: 2025-09-27
  file_id: '19525'
  file_name: 2025_JourNeuroscience_Stratigi.pdf
  file_size: 3111735
  relation: main_file
file_date_updated: 2025-09-27T22:30:02Z
has_accepted_license: '1'
intvolume: '        45'
isi: 1
issue: '13'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
  issn:
  - 0270-6474
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans
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: 45
year: '2025'
...
---
_id: '10826'
abstract:
- lang: eng
  text: Animals that lose one sensory modality often show augmented responses to other
    sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly
    understood. We probe such mechanisms by performing a forward genetic screen for
    mutants with enhanced O2 perception in Caenorhabditis elegans. Multiple mutants
    exhibiting increased O2 responsiveness concomitantly show defects in other sensory
    responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes
    pheromone-evoked Ca2+ responses in the ADL pheromone-sensing neurons. At the same
    time, ADL responsiveness to pre-synaptic input from O2-sensing neurons is heightened
    in qui-1, and other sensory defective mutants, resulting in enhanced neurosecretion
    although not increased Ca2+ responses. Expressing qui-1 selectively in ADL rescues
    both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling
    ADL neurons in qui-1 mutants highlights extensive changes in gene expression,
    notably of many neuropeptide receptors. We show that elevated ADL expression of
    the conserved neuropeptide receptor NPR-22 is necessary for enhanced ADL neurosecretion
    in qui-1 mutants, and is sufficient to confer increased ADL neurosecretion in
    control animals. Sensory loss can thus confer cross-modal plasticity by changing
    the peptidergic connectome.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: ScienComp
acknowledgement: "We would like to thank Gemma Chandratillake and Merav Cohen for
  identifying mutants and José David Moñino Sánchez for his help on neurosecretion
  assays. We are grateful to Kaveh Ashrafi (UCSF), Piali Sengupta (Brandeis), and
  the Caenorhabditis Genetic Center (funded by National Institutes of Health Infrastructure
  Program P40 OD010440) for strains and reagents ... and Rebecca Butcher (Univ. Florida)
  for C9 pheromone. We thank Tim Stevens, Paula Freire-Pritchett, Alastair Crisp,
  GurpreetGhattaoraya, and Fabian Amman for help with bioinformatic analysis, Ekaterina
  Lashmanova for help with injections, Iris Hardege for strains, and Isabel Beets
  (KU Leuven) and members of the de Bono Lab for comments on the manuscript. We thank
  the CRUK Cambridge Research Institute Genomics Core for next generation sequencing
  and the Flow Cytometry Facility at LMB for FACS. This research was supported by
  the Scientific Service Units (SSU) of IST Austria through resources provided by
  the Bioimaging Facility (BIF), the Life Science Facility (LSF) and Scientific Computing
  (SciCo-p– Bioinformatics).\r\nThis work was supported by the Medical Research Council
  UK (Studentship to GV), an\r\nAdvanced ERC grant (269,058 ACMO to MdB), and a Wellcome
  Investigator Award (209504/Z/17/Z to MdB)."
article_number: e68040
article_processing_charge: No
article_type: original
author:
- first_name: Giulio
  full_name: Valperga, Giulio
  id: 67F289DE-0D8F-11EA-9BDD-54AE3DDC885E
  last_name: Valperga
  orcid: 0000-0001-6726-3890
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Valperga G, de Bono M. Impairing one sensory modality enhances another by reconfiguring
    peptidergic signalling in Caenorhabditis elegans. <i>eLife</i>. 2022;11. doi:<a
    href="https://doi.org/10.7554/eLife.68040">10.7554/eLife.68040</a>
  apa: Valperga, G., &#38; de Bono, M. (2022). Impairing one sensory modality enhances
    another by reconfiguring peptidergic signalling in Caenorhabditis elegans. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.68040">https://doi.org/10.7554/eLife.68040</a>
  chicago: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances
    Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” <i>ELife</i>.
    eLife Sciences Publications, 2022. <a href="https://doi.org/10.7554/eLife.68040">https://doi.org/10.7554/eLife.68040</a>.
  ieee: G. Valperga and M. de Bono, “Impairing one sensory modality enhances another
    by reconfiguring peptidergic signalling in Caenorhabditis elegans,” <i>eLife</i>,
    vol. 11. eLife Sciences Publications, 2022.
  ista: Valperga G, de Bono M. 2022. Impairing one sensory modality enhances another
    by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 11,
    e68040.
  mla: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances
    Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” <i>ELife</i>,
    vol. 11, e68040, eLife Sciences Publications, 2022, doi:<a href="https://doi.org/10.7554/eLife.68040">10.7554/eLife.68040</a>.
  short: G. Valperga, M. de Bono, ELife 11 (2022).
corr_author: '1'
date_created: 2022-03-06T23:01:52Z
date_published: 2022-02-24T00:00:00Z
date_updated: 2026-04-02T12:45:39Z
day: '24'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.7554/eLife.68040
external_id:
  isi:
  - '000763432300001'
  pmid:
  - '35201977'
file:
- access_level: open_access
  checksum: cc1b9bf866d0f61f965556e0dd03d3ac
  content_type: application/pdf
  creator: dernst
  date_created: 2022-03-07T07:39:25Z
  date_updated: 2022-03-07T07:39:25Z
  file_id: '10830'
  file_name: 2022_eLife_Valperga.pdf
  file_size: 4095591
  relation: main_file
  success: 1
file_date_updated: 2022-03-07T07:39:25Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
publication: eLife
publication_identifier:
  eissn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Impairing one sensory modality enhances another by reconfiguring peptidergic
  signalling in Caenorhabditis elegans
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 11
year: '2022'
...
---
_id: '10846'
abstract:
- lang: eng
  text: The Golgi apparatus regulates the process of modification and subcellular
    localization of macromolecules, including proteins and lipids. Aberrant protein
    sorting caused by defects in the Golgi leads to various diseases in mammals. However,
    the role of the Golgi apparatus in organismal longevity remained largely unknown.
    By employing a quantitative proteomic approach, we demonstrated that MON-2, an
    evolutionarily conserved Arf-GEF protein implicated in Golgi-to-endosome trafficking,
    promotes longevity via upregulating macroautophagy/autophagy in C. elegans. Our
    data using cultured mammalian cells indicate that MON2 translocates from the Golgi
    to the endosome under starvation conditions, subsequently increasing autophagic
    flux by binding LGG-1/GABARAPL2. Thus, Golgi-to-endosome trafficking appears to
    be an evolutionarily conserved process for the upregulation of autophagy, which
    contributes to organismal longevity.
acknowledgement: This work is funded by National Research Foundation of Korea (NRF)
  grants NRF-2019R1A3B2067745 from the Korean Government (Ministry of Science and
  Information and Communications Technology (S-J.V.L.). NRF-2017R1A5A1015366 (S.Y.P,
  S-J.V.L). Korea Institute of Science and Technology (KIST) intramural grant (C.L).
article_processing_charge: No
article_type: original
author:
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Jooyeon
  full_name: Sohn, Jooyeon
  last_name: Sohn
- first_name: Cheolju
  full_name: Lee, Cheolju
  last_name: Lee
- first_name: Seung Yeol
  full_name: Park, Seung Yeol
  last_name: Park
- first_name: Seung Jae V.
  full_name: Lee, Seung Jae V.
  last_name: Lee
citation:
  ama: Artan M, Sohn J, Lee C, Park SY, Lee SJV. MON-2, a Golgi protein, promotes
    longevity by upregulating autophagy through mediating inter-organelle communications.
    <i>Autophagy</i>. 2022;18(5):1208-1210. doi:<a href="https://doi.org/10.1080/15548627.2022.2039523">10.1080/15548627.2022.2039523</a>
  apa: Artan, M., Sohn, J., Lee, C., Park, S. Y., &#38; Lee, S. J. V. (2022). MON-2,
    a Golgi protein, promotes longevity by upregulating autophagy through mediating
    inter-organelle communications. <i>Autophagy</i>. Taylor &#38; Francis. <a href="https://doi.org/10.1080/15548627.2022.2039523">https://doi.org/10.1080/15548627.2022.2039523</a>
  chicago: Artan, Murat, Jooyeon Sohn, Cheolju Lee, Seung Yeol Park, and Seung Jae
    V. Lee. “MON-2, a Golgi Protein, Promotes Longevity by Upregulating Autophagy
    through Mediating Inter-Organelle Communications.” <i>Autophagy</i>. Taylor &#38;
    Francis, 2022. <a href="https://doi.org/10.1080/15548627.2022.2039523">https://doi.org/10.1080/15548627.2022.2039523</a>.
  ieee: M. Artan, J. Sohn, C. Lee, S. Y. Park, and S. J. V. Lee, “MON-2, a Golgi protein,
    promotes longevity by upregulating autophagy through mediating inter-organelle
    communications,” <i>Autophagy</i>, vol. 18, no. 5. Taylor &#38; Francis, pp. 1208–1210,
    2022.
  ista: Artan M, Sohn J, Lee C, Park SY, Lee SJV. 2022. MON-2, a Golgi protein, promotes
    longevity by upregulating autophagy through mediating inter-organelle communications.
    Autophagy. 18(5), 1208–1210.
  mla: Artan, Murat, et al. “MON-2, a Golgi Protein, Promotes Longevity by Upregulating
    Autophagy through Mediating Inter-Organelle Communications.” <i>Autophagy</i>,
    vol. 18, no. 5, Taylor &#38; Francis, 2022, pp. 1208–10, doi:<a href="https://doi.org/10.1080/15548627.2022.2039523">10.1080/15548627.2022.2039523</a>.
  short: M. Artan, J. Sohn, C. Lee, S.Y. Park, S.J.V. Lee, Autophagy 18 (2022) 1208–1210.
date_created: 2022-03-13T23:01:47Z
date_published: 2022-02-19T00:00:00Z
date_updated: 2026-06-18T10:40:40Z
day: '19'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1080/15548627.2022.2039523
external_id:
  isi:
  - '000758859600001'
  pmid:
  - '35188063'
intvolume: '        18'
isi: 1
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1080/15548627.2022.2039523
month: '02'
oa: 1
oa_version: Published Version
page: 1208-1210
pmid: 1
publication: Autophagy
publication_identifier:
  eissn:
  - 1554-8635
  issn:
  - 1554-8627
publication_status: published
publisher: Taylor & Francis
quality_controlled: '1'
scopus_import: '1'
status: public
title: MON-2, a Golgi protein, promotes longevity by upregulating autophagy through
  mediating inter-organelle communications
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2022'
...
---
_id: '11456'
abstract:
- lang: eng
  text: The proteomes of specialized structures, and the interactomes of proteins
    of interest, provide entry points to elucidate the functions of molecular machines.
    Here, we review a proximity-labeling strategy that uses the improved E. coli biotin
    ligase TurboID to characterize C. elegans protein complexes. Although the focus
    is on C. elegans neurons, the method is applicable regardless of cell type. We
    describe detailed extraction procedures that solubilize the bulk of C. elegans
    proteins and highlight the importance of tagging endogenous genes, to ensure physiological
    expression levels. We review issues associated with non-specific background noise
    and the importance of appropriate controls. As proof of principle, we review our
    analysis of the interactome of a presynaptic active zone protein, ELKS-1. Our
    aim is to provide a detailed protocol for TurboID-based proximity labeling in
    C. elegans and to highlight its potential and its limitations to characterize
    protein complexes and subcellular compartments in this animal.
acknowledgement: We thank de Bono lab members for the helpful comments on the manuscript.
  The biotin-auxotrophic E. coli strain MG1655bioB:kan was a generous gift from J.
  Cronan (University of Illinois) and was kindly sent to us by Jessica Feldman and
  Ariana Sanchez (Stanford University). dg398 pEntryslot2_mNeongreen::3XFLAG::stop
  and dg397 pEntryslot3_mNeongreen::3XFLAG::stop::unc-54 3’UTR entry vector were kindly
  sent by Dr. Dominique Glauser (University of Fribourg). This work was supported
  by an Advanced ERC Grant (269058 ACMO) and a Wellcome Investigator Award (209504/Z/17/Z)
  to MdB and an ISTplus Fellowship to MA (Marie Sklodowska-Curie agreement No 754411).
alternative_title:
- Neuromethods
article_processing_charge: No
author:
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: 'Artan M, de Bono M. Proteomic Analysis of C. Elegans Neurons Using TurboID-Based
    Proximity Labeling. In: Yamamoto D, ed. <i>Behavioral Neurogenetics</i>. Vol 181.
    NM. New York: Springer Nature; 2022:277-294. doi:<a href="https://doi.org/10.1007/978-1-0716-2321-3_15">10.1007/978-1-0716-2321-3_15</a>'
  apa: 'Artan, M., &#38; de Bono, M. (2022). Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling. In D. Yamamoto (Ed.), <i>Behavioral Neurogenetics</i>
    (Vol. 181, pp. 277–294). New York: Springer Nature. <a href="https://doi.org/10.1007/978-1-0716-2321-3_15">https://doi.org/10.1007/978-1-0716-2321-3_15</a>'
  chicago: 'Artan, Murat, and Mario de Bono. “Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling.” In <i>Behavioral Neurogenetics</i>, edited
    by Daisuke Yamamoto, 181:277–94. NM. New York: Springer Nature, 2022. <a href="https://doi.org/10.1007/978-1-0716-2321-3_15">https://doi.org/10.1007/978-1-0716-2321-3_15</a>.'
  ieee: 'M. Artan and M. de Bono, “Proteomic Analysis of C. Elegans Neurons Using
    TurboID-Based Proximity Labeling,” in <i>Behavioral Neurogenetics</i>, vol. 181,
    D. Yamamoto, Ed. New York: Springer Nature, 2022, pp. 277–294.'
  ista: 'Artan M, de Bono M. 2022.Proteomic Analysis of C. Elegans Neurons Using TurboID-Based
    Proximity Labeling. In: Behavioral Neurogenetics. Neuromethods, vol. 181, 277–294.'
  mla: Artan, Murat, and Mario de Bono. “Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling.” <i>Behavioral Neurogenetics</i>, edited
    by Daisuke Yamamoto, vol. 181, Springer Nature, 2022, pp. 277–94, doi:<a href="https://doi.org/10.1007/978-1-0716-2321-3_15">10.1007/978-1-0716-2321-3_15</a>.
  short: M. Artan, M. de Bono, in:, D. Yamamoto (Ed.), Behavioral Neurogenetics, Springer
    Nature, New York, 2022, pp. 277–294.
corr_author: '1'
date_created: 2022-06-20T08:10:34Z
date_published: 2022-06-04T00:00:00Z
date_updated: 2025-04-14T07:43:58Z
day: '04'
department:
- _id: MaDe
doi: 10.1007/978-1-0716-2321-3_15
ec_funded: 1
editor:
- first_name: Daisuke
  full_name: Yamamoto, Daisuke
  last_name: Yamamoto
intvolume: '       181'
language:
- iso: eng
month: '06'
oa_version: None
page: 277-294
place: New York
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
publication: Behavioral Neurogenetics
publication_identifier:
  eisbn:
  - '9781071623213'
  eissn:
  - 1940-6045
  isbn:
  - '9781071623206'
  issn:
  - 0893-2336
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
series_title: NM
status: public
title: Proteomic Analysis of C. Elegans Neurons Using TurboID-Based Proximity Labeling
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 181
year: '2022'
...
---
_id: '11637'
abstract:
- lang: eng
  text: The ability to detect and respond to acute oxygen (O2) shortages is indispensable
    to aerobic life. The molecular mechanisms and circuits underlying this capacity
    are poorly understood. Here, we characterize the behavioral responses of feeding
    Caenorhabditis elegans to approximately 1% O2. Acute hypoxia triggers a bout of
    turning maneuvers followed by a persistent switch to rapid forward movement as
    animals seek to avoid and escape hypoxia. While the behavioral responses to 1%
    O2 closely resemble those evoked by 21% O2, they have distinct molecular and circuit
    underpinnings. Disrupting phosphodiesterases (PDEs), specific G proteins, or BBSome
    function inhibits escape from 1% O2 due to increased cGMP signaling. A primary
    source of cGMP is GCY-28, the ortholog of the atrial natriuretic peptide (ANP)
    receptor. cGMP activates the protein kinase G EGL-4 and enhances neuroendocrine
    secretion to inhibit acute responses to 1% O2. Triggering a rise in cGMP optogenetically
    in multiple neurons, including AIA interneurons, rapidly and reversibly inhibits
    escape from 1% O2. Ca2+ imaging reveals that a 7% to 1% O2 stimulus evokes a Ca2+
    decrease in several neurons. Defects in mitochondrial complex I (MCI) and mitochondrial
    complex I (MCIII), which lead to persistently high reactive oxygen species (ROS),
    abrogate acute hypoxia responses. In particular, repressing the expression of
    isp-1, which encodes the iron sulfur protein of MCIII, inhibits escape from 1%
    O2 without affecting responses to 21% O2. Both genetic and pharmacological up-regulation
    of mitochondrial ROS increase cGMP levels, which contribute to the reduced hypoxia
    responses. Our results implicate ROS and precise regulation of intracellular cGMP
    in the modulation of acute responses to hypoxia by C. elegans.
acknowledgement: ' This work was funded by H2020 European Research Council (ERC Advanced
  grant, 269058 ACMO, https://erc.europa.eu/funding/advanced-grants) and Wellcome
  Trust UK (Wellcome Investigator Award, 209504/Z/17/Z, https://wellcome.org/grant-funding/people-and-projects/grants-awarded/molecular-mechanisms-neural-circuit-function-0)
  to M.d.B, and by H2020 European Research Council (ERC starting grant, 802653 OXYGEN
  SENSING, https://erc.europa.eu/funding/starting-grants) and Vetenskapsrådet (VR
  starting grant, 2018-02216, https://www.vr.se/english.html) to C.C. The funders
  had no role in study design, data collection and analysis, decision to publish,
  or preparation of the manuscript.'
article_number: e3001684
article_processing_charge: No
article_type: original
author:
- first_name: Lina
  full_name: Zhao, Lina
  last_name: Zhao
- first_name: Lorenz A.
  full_name: Fenk, Lorenz A.
  last_name: Fenk
- first_name: Lars
  full_name: Nilsson, Lars
  last_name: Nilsson
- first_name: Niko Paresh
  full_name: Amin-Wetzel, Niko Paresh
  id: E95D3014-9D8C-11E9-9C80-D2F8E5697425
  last_name: Amin-Wetzel
- first_name: Nelson
  full_name: Ramirez, Nelson
  id: 39831956-E4FE-11E9-85DE-0DC7E5697425
  last_name: Ramirez
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
- first_name: Changchun
  full_name: Chen, Changchun
  last_name: Chen
citation:
  ama: Zhao L, Fenk LA, Nilsson L, et al. ROS and cGMP signaling modulate persistent
    escape from hypoxia in Caenorhabditis elegans. <i>PLoS Biology</i>. 2022;20(6).
    doi:<a href="https://doi.org/10.1371/journal.pbio.3001684">10.1371/journal.pbio.3001684</a>
  apa: Zhao, L., Fenk, L. A., Nilsson, L., Amin-Wetzel, N. P., Ramirez, N., de Bono,
    M., &#38; Chen, C. (2022). ROS and cGMP signaling modulate persistent escape from
    hypoxia in Caenorhabditis elegans. <i>PLoS Biology</i>. Public Library of Science.
    <a href="https://doi.org/10.1371/journal.pbio.3001684">https://doi.org/10.1371/journal.pbio.3001684</a>
  chicago: Zhao, Lina, Lorenz A. Fenk, Lars Nilsson, Niko Paresh Amin-Wetzel, Nelson
    Ramirez, Mario de Bono, and Changchun Chen. “ROS and CGMP Signaling Modulate Persistent
    Escape from Hypoxia in Caenorhabditis Elegans.” <i>PLoS Biology</i>. Public Library
    of Science, 2022. <a href="https://doi.org/10.1371/journal.pbio.3001684">https://doi.org/10.1371/journal.pbio.3001684</a>.
  ieee: L. Zhao <i>et al.</i>, “ROS and cGMP signaling modulate persistent escape
    from hypoxia in Caenorhabditis elegans,” <i>PLoS Biology</i>, vol. 20, no. 6.
    Public Library of Science, 2022.
  ista: Zhao L, Fenk LA, Nilsson L, Amin-Wetzel NP, Ramirez N, de Bono M, Chen C.
    2022. ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis
    elegans. PLoS Biology. 20(6), e3001684.
  mla: Zhao, Lina, et al. “ROS and CGMP Signaling Modulate Persistent Escape from
    Hypoxia in Caenorhabditis Elegans.” <i>PLoS Biology</i>, vol. 20, no. 6, e3001684,
    Public Library of Science, 2022, doi:<a href="https://doi.org/10.1371/journal.pbio.3001684">10.1371/journal.pbio.3001684</a>.
  short: L. Zhao, L.A. Fenk, L. Nilsson, N.P. Amin-Wetzel, N. Ramirez, M. de Bono,
    C. Chen, PLoS Biology 20 (2022).
corr_author: '1'
date_created: 2022-07-24T22:01:42Z
date_published: 2022-06-21T00:00:00Z
date_updated: 2025-04-15T07:32:21Z
day: '21'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1371/journal.pbio.3001684
external_id:
  isi:
  - '000828679600001'
  pmid:
  - '35727855'
file:
- access_level: open_access
  checksum: df4902f854ad76769d3203bfdc69f16c
  content_type: application/pdf
  creator: dernst
  date_created: 2022-07-25T07:38:49Z
  date_updated: 2022-07-25T07:38:49Z
  file_id: '11643'
  file_name: 2022_PLoSBiology_Zhao.pdf
  file_size: 3721585
  relation: main_file
  success: 1
file_date_updated: 2022-07-25T07:38:49Z
has_accepted_license: '1'
intvolume: '        20'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
publication: PLoS Biology
publication_identifier:
  eissn:
  - 1545-7885
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis
  elegans
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_id: '12082'
abstract:
- lang: eng
  text: Proximity-dependent protein labeling provides a powerful in vivo strategy
    to characterize the interactomes of specific proteins. We previously optimized
    a proximity labeling protocol for Caenorhabditis elegans using the highly active
    biotin ligase TurboID. A significant constraint on the sensitivity of TurboID
    is the presence of abundant endogenously biotinylated proteins that take up bandwidth
    in the mass spectrometer, notably carboxylases that use biotin as a cofactor.
    In C. elegans, these comprise POD-2/acetyl-CoA carboxylase alpha, PCCA-1/propionyl-CoA
    carboxylase alpha, PYC-1/pyruvate carboxylase, and MCCC-1/methylcrotonyl-CoA carboxylase
    alpha. Here, we developed ways to remove these carboxylases prior to streptavidin
    purification and mass spectrometry by engineering their corresponding genes to
    add a C-terminal His10 tag. This allows us to deplete them from C. elegans lysates
    using immobilized metal affinity chromatography. To demonstrate the method's efficacy,
    we use it to expand the interactome map of the presynaptic active zone protein
    ELKS-1. We identify many known active zone proteins, including UNC-10/RIM, SYD-2/liprin-alpha,
    SAD-1/BRSK1, CLA-1/CLArinet, C16E9.2/Sentryn, as well as previously uncharacterized
    potentially synaptic proteins such as the ortholog of human angiomotin, F59C12.3
    and the uncharacterized protein R148.3. Our approach provides a quick and inexpensive
    solution to a common contaminant problem in biotin-dependent proximity labeling.
    The approach may be applicable to other model organisms and will enable deeper
    and more complete analysis of interactors for proteins of interest.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank de Bono laboratory members for helpful comments on the
  article and the Mass Spec Facilities at IST Austria and Max Perutz Labs for invaluable
  discussions and comments on how to optimize mass spec analyses of worm samples.
  We are grateful to Ekaterina Lashmanova for designing the degron knock-in constructs
  and preparing the injection mixes for CRISPR/Cas9-mediated genome editing. All LC–MS/MS
  analyses were performed on instruments of the Vienna BioCenter Core Facilities instrument
  pool.\r\nThis work was supported by a Wellcome Investigator Award (grant no.: 209504/Z/17/Z
  ) to M.d.B. and an ISTplus Fellowship to M.A. (Marie Sklodowska-Curie agreement
  no.: 754411)."
article_number: '102343'
article_processing_charge: No
article_type: original
author:
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Markus
  full_name: Hartl, Markus
  last_name: Hartl
- first_name: Weiqiang
  full_name: Chen, Weiqiang
  last_name: Chen
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Artan M, Hartl M, Chen W, de Bono M. Depletion of endogenously biotinylated
    carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
    Caenorhabditis elegans. <i>Journal of Biological Chemistry</i>. 2022;298(9). doi:<a
    href="https://doi.org/10.1016/j.jbc.2022.102343">10.1016/j.jbc.2022.102343</a>
  apa: Artan, M., Hartl, M., Chen, W., &#38; de Bono, M. (2022). Depletion of endogenously
    biotinylated carboxylases enhances the sensitivity of TurboID-mediated proximity
    labeling in Caenorhabditis elegans. <i>Journal of Biological Chemistry</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.jbc.2022.102343">https://doi.org/10.1016/j.jbc.2022.102343</a>
  chicago: Artan, Murat, Markus Hartl, Weiqiang Chen, and Mario de Bono. “Depletion
    of Endogenously Biotinylated Carboxylases Enhances the Sensitivity of TurboID-Mediated
    Proximity Labeling in Caenorhabditis Elegans.” <i>Journal of Biological Chemistry</i>.
    Elsevier, 2022. <a href="https://doi.org/10.1016/j.jbc.2022.102343">https://doi.org/10.1016/j.jbc.2022.102343</a>.
  ieee: M. Artan, M. Hartl, W. Chen, and M. de Bono, “Depletion of endogenously biotinylated
    carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
    Caenorhabditis elegans,” <i>Journal of Biological Chemistry</i>, vol. 298, no.
    9. Elsevier, 2022.
  ista: Artan M, Hartl M, Chen W, de Bono M. 2022. Depletion of endogenously biotinylated
    carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
    Caenorhabditis elegans. Journal of Biological Chemistry. 298(9), 102343.
  mla: Artan, Murat, et al. “Depletion of Endogenously Biotinylated Carboxylases Enhances
    the Sensitivity of TurboID-Mediated Proximity Labeling in Caenorhabditis Elegans.”
    <i>Journal of Biological Chemistry</i>, vol. 298, no. 9, 102343, Elsevier, 2022,
    doi:<a href="https://doi.org/10.1016/j.jbc.2022.102343">10.1016/j.jbc.2022.102343</a>.
  short: M. Artan, M. Hartl, W. Chen, M. de Bono, Journal of Biological Chemistry
    298 (2022).
corr_author: '1'
date_created: 2022-09-11T22:01:55Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2025-04-14T07:44:00Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1016/j.jbc.2022.102343
ec_funded: 1
external_id:
  isi:
  - '000884241800011'
  pmid:
  - '35933017'
file:
- access_level: open_access
  checksum: e726c7b9315230e6710e0b1f1d1677e9
  content_type: application/pdf
  creator: dernst
  date_created: 2022-09-12T08:14:50Z
  date_updated: 2022-09-12T08:14:50Z
  file_id: '12092'
  file_name: 2022_JBC_Artan.pdf
  file_size: 2101656
  relation: main_file
  success: 1
file_date_updated: 2022-09-12T08:14:50Z
has_accepted_license: '1'
intvolume: '       298'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
publication: Journal of Biological Chemistry
publication_identifier:
  eissn:
  - 1083-351X
  issn:
  - 0021-9258
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Depletion of endogenously biotinylated carboxylases enhances the sensitivity
  of TurboID-mediated proximity labeling in Caenorhabditis elegans
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 298
year: '2022'
...
---
_id: '12275'
abstract:
- lang: eng
  text: N-glycans are molecularly diverse sugars borne by over 70% of proteins transiting
    the secretory pathway and have been implicated in protein folding, stability,
    and localization. Mutations in genes important for N-glycosylation result in congenital
    disorders of glycosylation that are often associated with intellectual disability.
    Here, we show that structurally distinct N-glycans regulate an extracellular protein
    complex involved in the patterning of somatosensory dendrites in Caenorhabditis
    elegans. Specifically, aman-2/Golgi alpha-mannosidase II, a conserved key enzyme
    in the biosynthesis of specific N-glycans, regulates the activity of the Menorin
    adhesion complex without obviously affecting the protein stability and localization
    of its components. AMAN-2 functions cell-autonomously to allow for decoration
    of the neuronal transmembrane receptor DMA-1/LRR-TM with the correct set of high-mannose/hybrid/paucimannose
    N-glycans. Moreover, distinct types of N-glycans on specific N-glycosylation sites
    regulate DMA-1/LRR-TM receptor function, which, together with three other extracellular
    proteins, forms the Menorin adhesion complex. In summary, specific N-glycan structures
    regulate dendrite patterning by coordinating the activity of an extracellular
    adhesion complex, suggesting that the molecular diversity of N-glycans can contribute
    to developmental specificity in the nervous system.
acknowledgement: 'We thank Scott Garforth, Sarah Garrett, Peri Kurshan, Yehuda Salzberg,
  PamelaStanley, Robert Townley, and members of the B€ulow laboratory for commentson
  the manuscript or helpful discussions during the course of this work. Wethank David
  Miller, Shohei Mitani, Kang Shen, and Iain Wilson for reagents,and Yuji Kohara for
  theyk11g705cDNA clone. We are grateful to MeeraTrivedi for sharing thedzIs117strain
  prior to publication. Some strains wereprovided by the Caenorhabditis Genome Center
  (funded by the NIH Office ofResearch Infrastructure Programs P40OD010440). This
  work was supportedby grants from the National Institute of Health (NIH): R01NS096672andR21NS111145to
  HEB; F31NS100370to MR; T32GM007288and F31HD066967to CADB; P30HD071593to Albert Einstein
  College of Medicine. We acknowl-edge support to MR by the Department of Neuroscience.
  NJRS was the recipi-ent of a Colciencias-Fulbright Fellowship and HEB of an Irma
  T. Hirschl/Monique Weill-Caulier research fellowship'
article_number: e54163
article_processing_charge: No
article_type: original
author:
- first_name: Maisha
  full_name: Rahman, Maisha
  last_name: Rahman
- first_name: Nelson
  full_name: Ramirez, Nelson
  id: 39831956-E4FE-11E9-85DE-0DC7E5697425
  last_name: Ramirez
- first_name: Carlos A
  full_name: Diaz‐Balzac, Carlos A
  last_name: Diaz‐Balzac
- first_name: Hannes E
  full_name: Bülow, Hannes E
  last_name: Bülow
citation:
  ama: Rahman M, Ramirez N, Diaz‐Balzac CA, Bülow HE. Specific N-glycans regulate
    an extracellular adhesion complex during somatosensory dendrite patterning. <i>EMBO
    Reports</i>. 2022;23(7). doi:<a href="https://doi.org/10.15252/embr.202154163">10.15252/embr.202154163</a>
  apa: Rahman, M., Ramirez, N., Diaz‐Balzac, C. A., &#38; Bülow, H. E. (2022). Specific
    N-glycans regulate an extracellular adhesion complex during somatosensory dendrite
    patterning. <i>EMBO Reports</i>. Embo Press. <a href="https://doi.org/10.15252/embr.202154163">https://doi.org/10.15252/embr.202154163</a>
  chicago: Rahman, Maisha, Nelson Ramirez, Carlos A Diaz‐Balzac, and Hannes E Bülow.
    “Specific N-Glycans Regulate an Extracellular Adhesion Complex during Somatosensory
    Dendrite Patterning.” <i>EMBO Reports</i>. Embo Press, 2022. <a href="https://doi.org/10.15252/embr.202154163">https://doi.org/10.15252/embr.202154163</a>.
  ieee: M. Rahman, N. Ramirez, C. A. Diaz‐Balzac, and H. E. Bülow, “Specific N-glycans
    regulate an extracellular adhesion complex during somatosensory dendrite patterning,”
    <i>EMBO Reports</i>, vol. 23, no. 7. Embo Press, 2022.
  ista: Rahman M, Ramirez N, Diaz‐Balzac CA, Bülow HE. 2022. Specific N-glycans regulate
    an extracellular adhesion complex during somatosensory dendrite patterning. EMBO
    Reports. 23(7), e54163.
  mla: Rahman, Maisha, et al. “Specific N-Glycans Regulate an Extracellular Adhesion
    Complex during Somatosensory Dendrite Patterning.” <i>EMBO Reports</i>, vol. 23,
    no. 7, e54163, Embo Press, 2022, doi:<a href="https://doi.org/10.15252/embr.202154163">10.15252/embr.202154163</a>.
  short: M. Rahman, N. Ramirez, C.A. Diaz‐Balzac, H.E. Bülow, EMBO Reports 23 (2022).
date_created: 2023-01-16T10:01:44Z
date_published: 2022-07-05T00:00:00Z
date_updated: 2026-06-18T17:26:25Z
day: '05'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.15252/embr.202154163
external_id:
  isi:
  - '000797302700001'
  pmid:
  - '35586945'
has_accepted_license: '1'
intvolume: '        23'
isi: 1
issue: '7'
keyword:
- Genetics
- Molecular Biology
- Biochemistry
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.15252/embr.202154163
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: EMBO Reports
publication_identifier:
  eissn:
  - 1469-3178
  issn:
  - 1469-221X
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Specific N-glycans regulate an extracellular adhesion complex during somatosensory
  dendrite patterning
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 23
year: '2022'
...
---
_id: '13069'
abstract:
- lang: eng
  text: To survive elevated temperatures, ectotherms adjust the fluidity of membranes
    by fine-tuning lipid desaturation levels in a process previously described to
    be cell-autonomous. We have discovered that, in Caenorhabditis elegans, neuronal
    Heat shock Factor 1 (HSF-1), the conserved master regulator of the heat shock
    response (HSR)- causes extensive fat remodelling in peripheral tissues. These
    changes include a decrease in fat desaturase and acid lipase expression in the
    intestine, and a global shift in the saturation levels of plasma membrane’s phospholipids.
    The observed remodelling of plasma membrane is in line with ectothermic adaptive
    responses and gives worms a cumulative advantage to warm temperatures. We have
    determined that at least six TAX-2/TAX-4 cGMP gated channel expressing sensory
    neurons and TGF-β/BMP are required for signalling across tissues to modulate fat
    desaturation. We also find neuronal hsf-1  is not only sufficient but also partially
    necessary to control the fat remodelling response and for survival at warm temperatures.
    This is the first study to show that a thermostat-based mechanism can cell non-autonomously
    coordinate membrane saturation and composition across tissues in a multicellular
    animal.
article_processing_charge: No
author:
- first_name: Laetitia
  full_name: Chauve, Laetitia
  last_name: Chauve
- first_name: Francesca
  full_name: Hodge, Francesca
  last_name: Hodge
- first_name: Sharlene
  full_name: Murdoch, Sharlene
  last_name: Murdoch
- first_name: Fatemah
  full_name: Masoudzadeh, Fatemah
  last_name: Masoudzadeh
- first_name: Harry-Jack
  full_name: Mann, Harry-Jack
  last_name: Mann
- first_name: Andrea
  full_name: Lopez-Clavijo, Andrea
  last_name: Lopez-Clavijo
- first_name: Hanneke
  full_name: Okkenhaug, Hanneke
  last_name: Okkenhaug
- first_name: Greg
  full_name: West, Greg
  last_name: West
- first_name: Bebiana C.
  full_name: Sousa, Bebiana C.
  last_name: Sousa
- first_name: Anne
  full_name: Segonds-Pichon, Anne
  last_name: Segonds-Pichon
- first_name: Cheryl
  full_name: Li, Cheryl
  last_name: Li
- first_name: Steven
  full_name: Wingett, Steven
  last_name: Wingett
- first_name: Hermine
  full_name: Kienberger, Hermine
  last_name: Kienberger
- first_name: Karin
  full_name: Kleigrewe, Karin
  last_name: Kleigrewe
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
- first_name: Michael
  full_name: Wakelam, Michael
  last_name: Wakelam
- first_name: Olivia
  full_name: Casanueva, Olivia
  last_name: Casanueva
citation:
  ama: Chauve L, Hodge F, Murdoch S, et al. Neuronal HSF-1 coordinates the propagation
    of fat desaturation across tissues to enable adaptation to high temperatures in
    C. elegans. 2021. doi:<a href="https://doi.org/10.5281/ZENODO.5519410">10.5281/ZENODO.5519410</a>
  apa: Chauve, L., Hodge, F., Murdoch, S., Masoudzadeh, F., Mann, H.-J., Lopez-Clavijo,
    A., … Casanueva, O. (2021). Neuronal HSF-1 coordinates the propagation of fat
    desaturation across tissues to enable adaptation to high temperatures in C. elegans.
    Zenodo. <a href="https://doi.org/10.5281/ZENODO.5519410">https://doi.org/10.5281/ZENODO.5519410</a>
  chicago: Chauve, Laetitia, Francesca Hodge, Sharlene Murdoch, Fatemah Masoudzadeh,
    Harry-Jack Mann, Andrea Lopez-Clavijo, Hanneke Okkenhaug, et al. “Neuronal HSF-1
    Coordinates the Propagation of Fat Desaturation across Tissues to Enable Adaptation
    to High Temperatures in C. Elegans.” Zenodo, 2021. <a href="https://doi.org/10.5281/ZENODO.5519410">https://doi.org/10.5281/ZENODO.5519410</a>.
  ieee: L. Chauve <i>et al.</i>, “Neuronal HSF-1 coordinates the propagation of fat
    desaturation across tissues to enable adaptation to high temperatures in C. elegans.”
    Zenodo, 2021.
  ista: Chauve L, Hodge F, Murdoch S, Masoudzadeh F, Mann H-J, Lopez-Clavijo A, Okkenhaug
    H, West G, Sousa BC, Segonds-Pichon A, Li C, Wingett S, Kienberger H, Kleigrewe
    K, de Bono M, Wakelam M, Casanueva O. 2021. Neuronal HSF-1 coordinates the propagation
    of fat desaturation across tissues to enable adaptation to high temperatures in
    C. elegans, Zenodo, <a href="https://doi.org/10.5281/ZENODO.5519410">10.5281/ZENODO.5519410</a>.
  mla: Chauve, Laetitia, et al. <i>Neuronal HSF-1 Coordinates the Propagation of Fat
    Desaturation across Tissues to Enable Adaptation to High Temperatures in C. Elegans</i>.
    Zenodo, 2021, doi:<a href="https://doi.org/10.5281/ZENODO.5519410">10.5281/ZENODO.5519410</a>.
  short: L. Chauve, F. Hodge, S. Murdoch, F. Masoudzadeh, H.-J. Mann, A. Lopez-Clavijo,
    H. Okkenhaug, G. West, B.C. Sousa, A. Segonds-Pichon, C. Li, S. Wingett, H. Kienberger,
    K. Kleigrewe, M. de Bono, M. Wakelam, O. Casanueva, (2021).
date_created: 2023-05-23T16:40:56Z
date_published: 2021-12-25T00:00:00Z
date_updated: 2023-08-14T11:53:26Z
day: '25'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.5281/ZENODO.5519410
main_file_link:
- open_access: '1'
  url: https://doi.org/10.5281/zenodo.5547464
month: '12'
oa: 1
oa_version: Published Version
publisher: Zenodo
related_material:
  record:
  - id: '10322'
    relation: used_in_publication
    status: public
status: public
title: Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues
  to enable adaptation to high temperatures in C. elegans
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_reference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2021'
...
---
_id: '15272'
abstract:
- lang: eng
  text: The assembly of neuronal circuits involves the migrations of neurons from
    their place of birth to their final location in the nervous system, as well as
    the coordinated growth and patterning of axons and dendrites. In screens for genes
    required for patterning of the nervous system, we identified the <jats:italic>catp-8/P5A-ATPase</jats:italic>
    as an important regulator of neural patterning. P5A-ATPases are part of the P-type
    ATPases, a family of proteins known to serve a conserved function as transporters
    of ions, lipids and polyamines in unicellular eukaryotes, plants, and humans.
    While the function of many P-type ATPases is relatively well understood, the function
    of P5A-ATPases in metazoans remained elusive. We show here, that the <jats:italic>Caenorhabditis
    elegans</jats:italic> ortholog <jats:italic>catp-8/P5A-ATPase</jats:italic> is
    required for defined aspects of nervous system development. Specifically, the
    <jats:italic>catp-8/P5A-ATPase</jats:italic> serves functions in shaping the elaborately
    sculpted dendritic trees of somatosensory PVD neurons. Moreover, <jats:italic>catp-8/P5A-ATPase</jats:italic>
    is required for axonal guidance and repulsion at the midline, as well as embryonic
    and postembryonic neuronal migrations. Interestingly, not all axons at the midline
    require <jats:italic>catp-8/P5A-ATPase</jats:italic>, although the axons run in
    the same fascicles and navigate the same space. Similarly, not all neuronal migrations
    require <jats:italic>catp-8/P5A-ATPase</jats:italic>. A CATP-8/P5A-ATPase reporter
    is localized to the ER in most, if not all, tissues and <jats:italic>catp-8/P5A-ATPase</jats:italic>
    can function both cell-autonomously and non-autonomously to regulate neuronal
    development. Genetic analyses establish that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    can function in multiple pathways, including the Menorin pathway, previously shown
    to control dendritic patterning in PVD, and Wnt signaling, which functions to
    control neuronal migrations. Lastly, we show that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    is required for localizing select transmembrane proteins necessary for dendrite
    morphogenesis. Collectively, our studies suggest that <jats:italic>catp-8/P5A-ATPase</jats:italic>
    serves diverse, yet specific, roles in different genetic pathways and may be involved
    in the regulation or localization of transmembrane and secreted proteins to specific
    subcellular compartments.
article_number: e1009475
article_processing_charge: No
article_type: original
author:
- first_name: Leo T. H.
  full_name: Tang, Leo T. H.
  last_name: Tang
- first_name: Meera
  full_name: Trivedi, Meera
  last_name: Trivedi
- first_name: Jenna
  full_name: Freund, Jenna
  last_name: Freund
- first_name: Christopher J.
  full_name: Salazar, Christopher J.
  last_name: Salazar
- first_name: Maisha
  full_name: Rahman, Maisha
  last_name: Rahman
- first_name: Nelson
  full_name: Ramirez, Nelson
  id: 39831956-E4FE-11E9-85DE-0DC7E5697425
  last_name: Ramirez
- first_name: Garrett
  full_name: Lee, Garrett
  last_name: Lee
- first_name: Yu
  full_name: Wang, Yu
  last_name: Wang
- first_name: Barth D.
  full_name: Grant, Barth D.
  last_name: Grant
- first_name: Hannes E.
  full_name: Bülow, Hannes E.
  last_name: Bülow
citation:
  ama: Tang LTH, Trivedi M, Freund J, et al. The CATP-8/P5A-type ATPase functions
    in multiple pathways during neuronal patterning. <i>PLOS Genetics</i>. 2021;17(7).
    doi:<a href="https://doi.org/10.1371/journal.pgen.1009475">10.1371/journal.pgen.1009475</a>
  apa: Tang, L. T. H., Trivedi, M., Freund, J., Salazar, C. J., Rahman, M., Ramirez,
    N., … Bülow, H. E. (2021). The CATP-8/P5A-type ATPase functions in multiple pathways
    during neuronal patterning. <i>PLOS Genetics</i>. Public Library of Science. <a
    href="https://doi.org/10.1371/journal.pgen.1009475">https://doi.org/10.1371/journal.pgen.1009475</a>
  chicago: Tang, Leo T. H., Meera Trivedi, Jenna Freund, Christopher J. Salazar, Maisha
    Rahman, Nelson Ramirez, Garrett Lee, Yu Wang, Barth D. Grant, and Hannes E. Bülow.
    “The CATP-8/P5A-Type ATPase Functions in Multiple Pathways during Neuronal Patterning.”
    <i>PLOS Genetics</i>. Public Library of Science, 2021. <a href="https://doi.org/10.1371/journal.pgen.1009475">https://doi.org/10.1371/journal.pgen.1009475</a>.
  ieee: L. T. H. Tang <i>et al.</i>, “The CATP-8/P5A-type ATPase functions in multiple
    pathways during neuronal patterning,” <i>PLOS Genetics</i>, vol. 17, no. 7. Public
    Library of Science, 2021.
  ista: Tang LTH, Trivedi M, Freund J, Salazar CJ, Rahman M, Ramirez N, Lee G, Wang
    Y, Grant BD, Bülow HE. 2021. The CATP-8/P5A-type ATPase functions in multiple
    pathways during neuronal patterning. PLOS Genetics. 17(7), e1009475.
  mla: Tang, Leo T. H., et al. “The CATP-8/P5A-Type ATPase Functions in Multiple Pathways
    during Neuronal Patterning.” <i>PLOS Genetics</i>, vol. 17, no. 7, e1009475, Public
    Library of Science, 2021, doi:<a href="https://doi.org/10.1371/journal.pgen.1009475">10.1371/journal.pgen.1009475</a>.
  short: L.T.H. Tang, M. Trivedi, J. Freund, C.J. Salazar, M. Rahman, N. Ramirez,
    G. Lee, Y. Wang, B.D. Grant, H.E. Bülow, PLOS Genetics 17 (2021).
date_created: 2024-04-03T07:57:12Z
date_published: 2021-07-01T00:00:00Z
date_updated: 2024-04-10T08:57:16Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1371/journal.pgen.1009475
external_id:
  pmid:
  - '34197450'
file:
- access_level: open_access
  checksum: 7352b195e4db6d404f702fe6ad8b55ad
  content_type: application/pdf
  creator: dernst
  date_created: 2024-04-10T08:53:43Z
  date_updated: 2024-04-10T08:53:43Z
  file_id: '15308'
  file_name: 2021_PlosGenetics_Tang.pdf
  file_size: 4224934
  relation: main_file
  success: 1
file_date_updated: 2024-04-10T08:53:43Z
has_accepted_license: '1'
intvolume: '        17'
issue: '7'
keyword:
- Cancer Research
- Genetics (clinical)
- Genetics
- Molecular Biology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
  issn:
  - 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: The CATP-8/P5A-type ATPase functions in multiple pathways during neuronal patterning
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2021'
...
---
_id: '10116'
abstract:
- lang: eng
  text: The ubiquitous Ca2+ sensor calmodulin (CaM) binds and regulates many proteins,
    including ion channels, CaM kinases, and calcineurin, according to Ca2+-CaM levels.
    What regulates neuronal CaM levels, is, however, unclear. CaM-binding transcription
    activators (CAMTAs) are ancient proteins expressed broadly in nervous systems
    and whose loss confers pleiotropic behavioral defects in flies, mice, and humans.
    Using Caenorhabditis elegans and Drosophila, we show that CAMTAs control neuronal
    CaM levels. The behavioral and neuronal Ca2+ signaling defects in mutants lacking
    camt-1, the sole C. elegans CAMTA, can be rescued by supplementing neuronal CaM.
    CAMT-1 binds multiple sites in the CaM promoter and deleting these sites phenocopies
    camt-1. Our data suggest CAMTAs mediate a conserved and general mechanism that
    controls neuronal CaM levels, thereby regulating Ca2+ signaling, physiology, and
    behavior.
acknowledgement: The authors thank the MRC-LMB Flow Cytometry facility and Imaging
  Service for support, the Cancer Research UK Cambridge Institute Genomics Core for
  Next Generation Sequencing, Julie Ahringer and Alex Appert for advice and technical
  help for ChIP-seq experiments, Paula Freire-Pritchett, Tim Stevens, and Gurpreet
  Ghattaoraya for RNA-seq and ChIP-seq analyses, Nikos Chronis for the TN-XL plasmid,
  Hong-Sheng Li and Daisuke Yamamoto for generously sending the tes2 and cro mutants,
  Daria Siekhaus for hosting the fly work, Michaela Misova for technical assistance.
  The authors are very grateful to Salihah Ece Sönmez for teaching us how to dissect,
  mount and stain Drosophila retinae. This work was supported by an Advanced ERC grant
  (269058 ACMO) and a Wellcome Investigator Award (209504/Z/17/Z) to MdB, and an IST
  Plus Fellowship to TV-B (Marie Sklodowska-Curie Agreement no 754411).
article_number: e68238
article_processing_charge: No
article_type: original
author:
- first_name: Thanh
  full_name: Vuong-Brender, Thanh
  id: D389312E-10C4-11EA-ABF4-A4B43DDC885E
  last_name: Vuong-Brender
- first_name: Sean
  full_name: Flynn, Sean
  last_name: Flynn
- first_name: Yvonne
  full_name: Vallis, Yvonne
  id: 05A2795C-31B5-11EA-83A7-7DA23DDC885E
  last_name: Vallis
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Vuong-Brender T, Flynn S, Vallis Y, de Bono M. Neuronal calmodulin levels are
    controlled by CAMTA transcription factors. <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/eLife.68238">10.7554/eLife.68238</a>
  apa: Vuong-Brender, T., Flynn, S., Vallis, Y., &#38; de Bono, M. (2021). Neuronal
    calmodulin levels are controlled by CAMTA transcription factors. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.68238">https://doi.org/10.7554/eLife.68238</a>
  chicago: Vuong-Brender, Thanh, Sean Flynn, Yvonne Vallis, and Mario de Bono. “Neuronal
    Calmodulin Levels Are Controlled by CAMTA Transcription Factors.” <i>ELife</i>.
    eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/eLife.68238">https://doi.org/10.7554/eLife.68238</a>.
  ieee: T. Vuong-Brender, S. Flynn, Y. Vallis, and M. de Bono, “Neuronal calmodulin
    levels are controlled by CAMTA transcription factors,” <i>eLife</i>, vol. 10.
    eLife Sciences Publications, 2021.
  ista: Vuong-Brender T, Flynn S, Vallis Y, de Bono M. 2021. Neuronal calmodulin levels
    are controlled by CAMTA transcription factors. eLife. 10, e68238.
  mla: Vuong-Brender, Thanh, et al. “Neuronal Calmodulin Levels Are Controlled by
    CAMTA Transcription Factors.” <i>ELife</i>, vol. 10, e68238, eLife Sciences Publications,
    2021, doi:<a href="https://doi.org/10.7554/eLife.68238">10.7554/eLife.68238</a>.
  short: T. Vuong-Brender, S. Flynn, Y. Vallis, M. de Bono, ELife 10 (2021).
date_created: 2021-10-10T22:01:22Z
date_published: 2021-09-17T00:00:00Z
date_updated: 2025-04-14T07:43:46Z
day: '17'
ddc:
- '610'
department:
- _id: MaDe
doi: 10.7554/eLife.68238
ec_funded: 1
external_id:
  isi:
  - '000695716100001'
  pmid:
  - '34499028'
file:
- access_level: open_access
  checksum: b465e172d2b1f57aa26a2571a085d052
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-10-11T14:15:07Z
  date_updated: 2021-10-11T14:15:07Z
  file_id: '10122'
  file_name: 2021_eLife_VuongBrender.pdf
  file_size: 1774624
  relation: main_file
  success: 1
file_date_updated: 2021-10-11T14:15:07Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
publication: eLife
publication_identifier:
  eissn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neuronal calmodulin levels are controlled by CAMTA transcription factors
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '10117'
abstract:
- lang: eng
  text: Proximity labeling provides a powerful in vivo tool to characterize the proteome
    of subcellular structures and the interactome of specific proteins. The nematode
    Caenorhabditis elegans is one of the most intensely studied organisms in biology,
    offering many advantages for biochemistry. Using the highly active biotin ligase
    TurboID, we optimize here a proximity labeling protocol for C. elegans. An advantage
    of TurboID is that biotin's high affinity for streptavidin means biotin-labeled
    proteins can be affinity-purified under harsh denaturing conditions. By combining
    extensive sonication with aggressive denaturation using SDS and urea, we achieved
    near-complete solubilization of worm proteins. We then used this protocol to characterize
    the proteomes of the worm gut, muscle, skin, and nervous system. Neurons are among
    the smallest C. elegans cells. To probe the method's sensitivity, we expressed
    TurboID exclusively in the two AFD neurons and showed that the protocol could
    identify known and previously unknown proteins expressed selectively in AFD. The
    active zones of synapses are composed of a protein matrix that is difficult to
    solubilize and purify. To test if our protocol could solubilize active zone proteins,
    we knocked TurboID into the endogenous elks-1 gene, which encodes a presynaptic
    active zone protein. We identified many known ELKS-1-interacting active zone proteins,
    as well as previously uncharacterized synaptic proteins. Versatile vectors and
    the inherent advantages of using C. elegans, including fast growth and the ability
    to rapidly make and functionally test knock-ins, make proximity labeling a valuable
    addition to the armory of this model organism.
acknowledgement: We thank de Bono lab members for helpful comments on the manuscript,
  IST Austria and University of Vienna Mass Spec Facilities for invaluable discussions
  and comments for the optimization of mass spec analyses of worm samples. The biotin
  auxotropic E. coli strain MG1655bioB:kan was gift from John Cronan (University of
  Illinois) and was kindly sent to us by Jessica Feldman and Ariana Sanchez (Stanford
  University). dg398 pEntryslot2_mNeongreen::3XFLAG::stop and dg397 pEntryslot3_mNeongreen::3XFLAG::stop::unc-54
  3′UTR entry vector were kindly shared by Dr Dominique Glauser (University of Fribourg).
  Codon-optimized mScarlet vector was a generous gift from Dr Manuel Zimmer (University
  of Vienna).
article_number: '101094'
article_processing_charge: Yes
article_type: original
author:
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Stephen
  full_name: Barratt, Stephen
  id: 57740d2b-2a88-11ec-97cf-d9e6d1b39677
  last_name: Barratt
- first_name: Sean M.
  full_name: Flynn, Sean M.
  last_name: Flynn
- first_name: Farida
  full_name: Begum, Farida
  last_name: Begum
- first_name: Mark
  full_name: Skehel, Mark
  last_name: Skehel
- first_name: Armel
  full_name: Nicolas, Armel
  id: 2A103192-F248-11E8-B48F-1D18A9856A87
  last_name: Nicolas
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Artan M, Barratt S, Flynn SM, et al. Interactome analysis of Caenorhabditis
    elegans synapses by TurboID-based proximity labeling. <i>Journal of Biological
    Chemistry</i>. 2021;297(3). doi:<a href="https://doi.org/10.1016/J.JBC.2021.101094">10.1016/J.JBC.2021.101094</a>
  apa: Artan, M., Barratt, S., Flynn, S. M., Begum, F., Skehel, M., Nicolas, A., &#38;
    de Bono, M. (2021). Interactome analysis of Caenorhabditis elegans synapses by
    TurboID-based proximity labeling. <i>Journal of Biological Chemistry</i>. Elsevier.
    <a href="https://doi.org/10.1016/J.JBC.2021.101094">https://doi.org/10.1016/J.JBC.2021.101094</a>
  chicago: Artan, Murat, Stephen Barratt, Sean M. Flynn, Farida Begum, Mark Skehel,
    Armel Nicolas, and Mario de Bono. “Interactome Analysis of Caenorhabditis Elegans
    Synapses by TurboID-Based Proximity Labeling.” <i>Journal of Biological Chemistry</i>.
    Elsevier, 2021. <a href="https://doi.org/10.1016/J.JBC.2021.101094">https://doi.org/10.1016/J.JBC.2021.101094</a>.
  ieee: M. Artan <i>et al.</i>, “Interactome analysis of Caenorhabditis elegans synapses
    by TurboID-based proximity labeling,” <i>Journal of Biological Chemistry</i>,
    vol. 297, no. 3. Elsevier, 2021.
  ista: Artan M, Barratt S, Flynn SM, Begum F, Skehel M, Nicolas A, de Bono M. 2021.
    Interactome analysis of Caenorhabditis elegans synapses by TurboID-based proximity
    labeling. Journal of Biological Chemistry. 297(3), 101094.
  mla: Artan, Murat, et al. “Interactome Analysis of Caenorhabditis Elegans Synapses
    by TurboID-Based Proximity Labeling.” <i>Journal of Biological Chemistry</i>,
    vol. 297, no. 3, 101094, Elsevier, 2021, doi:<a href="https://doi.org/10.1016/J.JBC.2021.101094">10.1016/J.JBC.2021.101094</a>.
  short: M. Artan, S. Barratt, S.M. Flynn, F. Begum, M. Skehel, A. Nicolas, M. de
    Bono, Journal of Biological Chemistry 297 (2021).
date_created: 2021-10-10T22:01:23Z
date_published: 2021-09-01T00:00:00Z
date_updated: 2025-04-14T07:43:46Z
day: '01'
ddc:
- '612'
department:
- _id: MaDe
- _id: LifeSc
doi: 10.1016/J.JBC.2021.101094
ec_funded: 1
external_id:
  isi:
  - '000706409200006'
file:
- access_level: open_access
  checksum: 19e39d36c5b9387c6dc0e89c9ae856ab
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-10-11T12:20:58Z
  date_updated: 2021-10-11T12:20:58Z
  file_id: '10121'
  file_name: 2021_JBC_Artan.pdf
  file_size: 1680010
  relation: main_file
  success: 1
file_date_updated: 2021-10-11T12:20:58Z
has_accepted_license: '1'
intvolume: '       297'
isi: 1
issue: '3'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
publication: Journal of Biological Chemistry
publication_identifier:
  eissn:
  - 1083-351X
  issn:
  - 0021-9258
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Interactome analysis of Caenorhabditis elegans synapses by TurboID-based proximity
  labeling
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 297
year: '2021'
...
---
_id: '10322'
abstract:
- lang: eng
  text: To survive elevated temperatures, ectotherms adjust the fluidity of membranes
    by fine-tuning lipid desaturation levels in a process previously described to
    be cell autonomous. We have discovered that, in Caenorhabditis elegans, neuronal
    heat shock factor 1 (HSF-1), the conserved master regulator of the heat shock
    response (HSR), causes extensive fat remodeling in peripheral tissues. These changes
    include a decrease in fat desaturase and acid lipase expression in the intestine
    and a global shift in the saturation levels of plasma membrane’s phospholipids.
    The observed remodeling of plasma membrane is in line with ectothermic adaptive
    responses and gives worms a cumulative advantage to warm temperatures. We have
    determined that at least 6 TAX-2/TAX-4 cyclic guanosine monophosphate (cGMP) gated
    channel expressing sensory neurons, and transforming growth factor ß (TGF-β)/bone
    morphogenetic protein (BMP) are required for signaling across tissues to modulate
    fat desaturation. We also find neuronal hsf-1 is not only sufficient but also
    partially necessary to control the fat remodeling response and for survival at
    warm temperatures. This is the first study to show that a thermostat-based mechanism
    can cell nonautonomously coordinate membrane saturation and composition across
    tissues in a multicellular animal.
acknowledgement: We dedicate this work to the memory of Michael J.O. Wakelam. We would
  like to acknowledge Michael Fasseas (Invermis, Magnitude Biosciences) for plasmid
  injections and Sunny Biotech for transgenics; Catalina Vallejos and John Marioni
  for statistical advice at the beginning of the work; Simon Walker, Imaging, Bioinformatics
  and Lipidomics Facilities at Babraham Institute for technical support; and Cindy
  Voisine, Michael Witting, Jon Houseley, Len Stephens, Carmen Nussbaum Krammer, Rebeca
  Aldunate, Patricija van Oosten-Hawle, Jean-Louis Bessereau, and Jane Alfred for
  feedback on the manuscript. We thank Andy Dillin, Atsushi Kuhara, Amy Walker, Andrew
  Leifer, Yun Zhang, and Michalis Barkoulas for reagents and Julie Ahringer, Anne
  Ferguson-Smith, and Anne Corcoran for support and helpful discussions. We also acknowledge
  Babraham Institute Facilities.
article_number: e3001431
article_processing_charge: No
article_type: original
author:
- first_name: Laetitia
  full_name: Chauve, Laetitia
  last_name: Chauve
- first_name: Francesca
  full_name: Hodge, Francesca
  last_name: Hodge
- first_name: Sharlene
  full_name: Murdoch, Sharlene
  last_name: Murdoch
- first_name: Fatemah
  full_name: Masoudzadeh, Fatemah
  last_name: Masoudzadeh
- first_name: Harry Jack
  full_name: Mann, Harry Jack
  last_name: Mann
- first_name: Andrea
  full_name: Lopez-Clavijo, Andrea
  last_name: Lopez-Clavijo
- first_name: Hanneke
  full_name: Okkenhaug, Hanneke
  last_name: Okkenhaug
- first_name: Greg
  full_name: West, Greg
  last_name: West
- first_name: Bebiana C.
  full_name: Sousa, Bebiana C.
  last_name: Sousa
- first_name: Anne
  full_name: Segonds-Pichon, Anne
  last_name: Segonds-Pichon
- first_name: Cheryl
  full_name: Li, Cheryl
  last_name: Li
- first_name: Steven
  full_name: Wingett, Steven
  last_name: Wingett
- first_name: Hermine
  full_name: Kienberger, Hermine
  last_name: Kienberger
- first_name: Karin
  full_name: Kleigrewe, Karin
  last_name: Kleigrewe
- first_name: Mario
  full_name: De Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: De Bono
  orcid: 0000-0001-8347-0443
- first_name: Michael
  full_name: Wakelam, Michael
  last_name: Wakelam
- first_name: Olivia
  full_name: Casanueva, Olivia
  last_name: Casanueva
citation:
  ama: Chauve L, Hodge F, Murdoch S, et al. Neuronal HSF-1 coordinates the propagation
    of fat desaturation across tissues to enable adaptation to high temperatures in
    C. elegans. <i>PLoS Biology</i>. 2021;19(11). doi:<a href="https://doi.org/10.1371/journal.pbio.3001431">10.1371/journal.pbio.3001431</a>
  apa: Chauve, L., Hodge, F., Murdoch, S., Masoudzadeh, F., Mann, H. J., Lopez-Clavijo,
    A., … Casanueva, O. (2021). Neuronal HSF-1 coordinates the propagation of fat
    desaturation across tissues to enable adaptation to high temperatures in C. elegans.
    <i>PLoS Biology</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pbio.3001431">https://doi.org/10.1371/journal.pbio.3001431</a>
  chicago: Chauve, Laetitia, Francesca Hodge, Sharlene Murdoch, Fatemah Masoudzadeh,
    Harry Jack Mann, Andrea Lopez-Clavijo, Hanneke Okkenhaug, et al. “Neuronal HSF-1
    Coordinates the Propagation of Fat Desaturation across Tissues to Enable Adaptation
    to High Temperatures in C. Elegans.” <i>PLoS Biology</i>. Public Library of Science,
    2021. <a href="https://doi.org/10.1371/journal.pbio.3001431">https://doi.org/10.1371/journal.pbio.3001431</a>.
  ieee: L. Chauve <i>et al.</i>, “Neuronal HSF-1 coordinates the propagation of fat
    desaturation across tissues to enable adaptation to high temperatures in C. elegans,”
    <i>PLoS Biology</i>, vol. 19, no. 11. Public Library of Science, 2021.
  ista: Chauve L, Hodge F, Murdoch S, Masoudzadeh F, Mann HJ, Lopez-Clavijo A, Okkenhaug
    H, West G, Sousa BC, Segonds-Pichon A, Li C, Wingett S, Kienberger H, Kleigrewe
    K, de Bono M, Wakelam M, Casanueva O. 2021. Neuronal HSF-1 coordinates the propagation
    of fat desaturation across tissues to enable adaptation to high temperatures in
    C. elegans. PLoS Biology. 19(11), e3001431.
  mla: Chauve, Laetitia, et al. “Neuronal HSF-1 Coordinates the Propagation of Fat
    Desaturation across Tissues to Enable Adaptation to High Temperatures in C. Elegans.”
    <i>PLoS Biology</i>, vol. 19, no. 11, e3001431, Public Library of Science, 2021,
    doi:<a href="https://doi.org/10.1371/journal.pbio.3001431">10.1371/journal.pbio.3001431</a>.
  short: L. Chauve, F. Hodge, S. Murdoch, F. Masoudzadeh, H.J. Mann, A. Lopez-Clavijo,
    H. Okkenhaug, G. West, B.C. Sousa, A. Segonds-Pichon, C. Li, S. Wingett, H. Kienberger,
    K. Kleigrewe, M. de Bono, M. Wakelam, O. Casanueva, PLoS Biology 19 (2021).
date_created: 2021-11-21T23:01:28Z
date_published: 2021-11-01T00:00:00Z
date_updated: 2023-08-14T11:53:27Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1371/journal.pbio.3001431
external_id:
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publication: PLoS Biology
publication_identifier:
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  - 1545-7885
  issn:
  - 1544-9173
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
  record:
  - id: '13069'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues
  to enable adaptation to high temperatures in C. elegans
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 19
year: '2021'
...
---
_id: '15057'
abstract:
- lang: eng
  text: Vaccinia virus–related kinase (VRK) is an evolutionarily conserved nuclear
    protein kinase. VRK-1, the single Caenorhabditis elegans VRK ortholog, functions
    in cell division and germline proliferation. However, the role of VRK-1 in postmitotic
    cells and adult life span remains unknown. Here, we show that VRK-1 increases
    organismal longevity by activating the cellular energy sensor, AMP-activated protein
    kinase (AMPK), via direct phosphorylation. We found that overexpression of vrk-1
    in the soma of adult C. elegans increased life span and, conversely, inhibition
    of vrk-1 decreased life span. In addition, vrk-1 was required for longevity conferred
    by mutations that inhibit C. elegans mitochondrial respiration, which requires
    AMPK. VRK-1 directly phosphorylated and up-regulated AMPK in both C. elegans and
    cultured human cells. Thus, our data show that the somatic nuclear kinase, VRK-1,
    promotes longevity through AMPK activation, and this function appears to be conserved
    between C. elegans and humans.
acknowledgement: 'This research was supported by grants NRF-2019R1A3B2067745 and NRF-2017R1A5A1015366
  funded by the Korean Government (MSIT) through the National Research Foundation
  (NRF) of Korea to S.-J.V.L. and by grant Basic Science Research Program (No. 2019R1A2C2009440)
  funded by the Korean Government (MSIT) through the NRF of Korea to K.-T.K. '
article_number: aaw7824
article_processing_charge: No
article_type: original
author:
- first_name: Sangsoon
  full_name: Park, Sangsoon
  last_name: Park
- first_name: Murat
  full_name: Artan, Murat
  id: C407B586-6052-11E9-B3AE-7006E6697425
  last_name: Artan
  orcid: 0000-0001-8945-6992
- first_name: Seung Hyun
  full_name: Han, Seung Hyun
  last_name: Han
- first_name: Hae-Eun H.
  full_name: Park, Hae-Eun H.
  last_name: Park
- first_name: Yoonji
  full_name: Jung, Yoonji
  last_name: Jung
- first_name: Ara B.
  full_name: Hwang, Ara B.
  last_name: Hwang
- first_name: Won Sik
  full_name: Shin, Won Sik
  last_name: Shin
- first_name: Kyong-Tai
  full_name: Kim, Kyong-Tai
  last_name: Kim
- first_name: Seung-Jae V.
  full_name: Lee, Seung-Jae V.
  last_name: Lee
citation:
  ama: Park S, Artan M, Han SH, et al. VRK-1 extends life span by activation of AMPK
    via phosphorylation. <i>Science Advances</i>. 2020;6(27). doi:<a href="https://doi.org/10.1126/sciadv.aaw7824">10.1126/sciadv.aaw7824</a>
  apa: Park, S., Artan, M., Han, S. H., Park, H.-E. H., Jung, Y., Hwang, A. B., …
    Lee, S.-J. V. (2020). VRK-1 extends life span by activation of AMPK via phosphorylation.
    <i>Science Advances</i>. American Association for the Advancement of Science.
    <a href="https://doi.org/10.1126/sciadv.aaw7824">https://doi.org/10.1126/sciadv.aaw7824</a>
  chicago: Park, Sangsoon, Murat Artan, Seung Hyun Han, Hae-Eun H. Park, Yoonji Jung,
    Ara B. Hwang, Won Sik Shin, Kyong-Tai Kim, and Seung-Jae V. Lee. “VRK-1 Extends
    Life Span by Activation of AMPK via Phosphorylation.” <i>Science Advances</i>.
    American Association for the Advancement of Science, 2020. <a href="https://doi.org/10.1126/sciadv.aaw7824">https://doi.org/10.1126/sciadv.aaw7824</a>.
  ieee: S. Park <i>et al.</i>, “VRK-1 extends life span by activation of AMPK via
    phosphorylation,” <i>Science Advances</i>, vol. 6, no. 27. American Association
    for the Advancement of Science, 2020.
  ista: Park S, Artan M, Han SH, Park H-EH, Jung Y, Hwang AB, Shin WS, Kim K-T, Lee
    S-JV. 2020. VRK-1 extends life span by activation of AMPK via phosphorylation.
    Science Advances. 6(27), aaw7824.
  mla: Park, Sangsoon, et al. “VRK-1 Extends Life Span by Activation of AMPK via Phosphorylation.”
    <i>Science Advances</i>, vol. 6, no. 27, aaw7824, American Association for the
    Advancement of Science, 2020, doi:<a href="https://doi.org/10.1126/sciadv.aaw7824">10.1126/sciadv.aaw7824</a>.
  short: S. Park, M. Artan, S.H. Han, H.-E.H. Park, Y. Jung, A.B. Hwang, W.S. Shin,
    K.-T. Kim, S.-J.V. Lee, Science Advances 6 (2020).
date_created: 2024-03-04T09:41:57Z
date_published: 2020-07-01T00:00:00Z
date_updated: 2024-03-04T09:52:09Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1126/sciadv.aaw7824
file:
- access_level: open_access
  checksum: a37157cd0de709dce5fe03f4a31cd0b6
  content_type: application/pdf
  creator: dernst
  date_created: 2024-03-04T09:46:41Z
  date_updated: 2024-03-04T09:46:41Z
  file_id: '15058'
  file_name: 2020_ScienceAdvances_Park.pdf
  file_size: 1864415
  relation: main_file
  success: 1
file_date_updated: 2024-03-04T09:46:41Z
has_accepted_license: '1'
intvolume: '         6'
issue: '27'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '07'
oa: 1
oa_version: Published Version
publication: Science Advances
publication_identifier:
  eissn:
  - 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
status: public
title: VRK-1 extends life span by activation of AMPK via phosphorylation
tmp:
  image: /images/cc_by_nc.png
  legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
  short: CC BY-NC (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2020'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '19306'
acknowledgement: "We thank Maureen Barr, Martin Harterink, Max Heiman and Inna Nechipurenko
  for reagents, the Caenorhabditis Genetics Center for strains, and the Sengupta lab
  for comments and advice.\r\nThis work was funded in part by the NIH (R35 GM122463
  – P.S., and F32 DC018453 – A.P.), and the EMBO (ALTF 302-2019 – N.A-W.)."
article_number: '303'
article_processing_charge: Yes
article_type: original
author:
- first_name: Anna
  full_name: Kazatskaya, Anna
  last_name: Kazatskaya
- first_name: Lisa
  full_name: Yuan, Lisa
  last_name: Yuan
- first_name: Niko Paresh
  full_name: Amin-Wetzel, Niko Paresh
  id: E95D3014-9D8C-11E9-9C80-D2F8E5697425
  last_name: Amin-Wetzel
- first_name: Alison
  full_name: Philbrook, Alison
  last_name: Philbrook
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
- first_name: Piali
  full_name: Sengupta, Piali
  last_name: Sengupta
citation:
  ama: Kazatskaya A, Yuan L, Amin-Wetzel NP, Philbrook A, de Bono M, Sengupta P. The
    URX oxygen-sensing neurons in C. elegans are ciliated. <i>microPublication Biology</i>.
    2020;2020(9). doi:<a href="https://doi.org/10.17912/MICROPUB.BIOLOGY.000303">10.17912/MICROPUB.BIOLOGY.000303</a>
  apa: Kazatskaya, A., Yuan, L., Amin-Wetzel, N. P., Philbrook, A., de Bono, M., &#38;
    Sengupta, P. (2020). The URX oxygen-sensing neurons in C. elegans are ciliated.
    <i>MicroPublication Biology</i>. Caltech Library. <a href="https://doi.org/10.17912/MICROPUB.BIOLOGY.000303">https://doi.org/10.17912/MICROPUB.BIOLOGY.000303</a>
  chicago: Kazatskaya, Anna, Lisa Yuan, Niko Paresh Amin-Wetzel, Alison Philbrook,
    Mario de Bono, and Piali Sengupta. “The URX Oxygen-Sensing Neurons in C. Elegans
    Are Ciliated.” <i>MicroPublication Biology</i>. Caltech Library, 2020. <a href="https://doi.org/10.17912/MICROPUB.BIOLOGY.000303">https://doi.org/10.17912/MICROPUB.BIOLOGY.000303</a>.
  ieee: A. Kazatskaya, L. Yuan, N. P. Amin-Wetzel, A. Philbrook, M. de Bono, and P.
    Sengupta, “The URX oxygen-sensing neurons in C. elegans are ciliated,” <i>microPublication
    Biology</i>, vol. 2020, no. 9. Caltech Library, 2020.
  ista: Kazatskaya A, Yuan L, Amin-Wetzel NP, Philbrook A, de Bono M, Sengupta P.
    2020. The URX oxygen-sensing neurons in C. elegans are ciliated. microPublication
    Biology. 2020(9), 303.
  mla: Kazatskaya, Anna, et al. “The URX Oxygen-Sensing Neurons in C. Elegans Are
    Ciliated.” <i>MicroPublication Biology</i>, vol. 2020, no. 9, 303, Caltech Library,
    2020, doi:<a href="https://doi.org/10.17912/MICROPUB.BIOLOGY.000303">10.17912/MICROPUB.BIOLOGY.000303</a>.
  short: A. Kazatskaya, L. Yuan, N.P. Amin-Wetzel, A. Philbrook, M. de Bono, P. Sengupta,
    MicroPublication Biology 2020 (2020).
date_created: 2025-03-07T08:21:51Z
date_published: 2020-09-20T00:00:00Z
date_updated: 2025-03-11T08:30:41Z
day: '20'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.17912/MICROPUB.BIOLOGY.000303
external_id:
  pmid:
  - '33005885'
file:
- access_level: open_access
  checksum: 14a7cad20775521ce85e0e3c77aa7936
  content_type: application/pdf
  creator: dernst
  date_created: 2025-03-11T08:27:40Z
  date_updated: 2025-03-11T08:27:40Z
  file_id: '19383'
  file_name: 2020_MicroPublBio_Kazatskaya.pdf
  file_size: 1486239
  relation: main_file
  success: 1
file_date_updated: 2025-03-11T08:27:40Z
has_accepted_license: '1'
intvolume: '      2020'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: microPublication Biology
publication_identifier:
  eissn:
  - 2578-9430
publication_status: published
publisher: Caltech Library
quality_controlled: '1'
status: public
title: The URX oxygen-sensing neurons in C. elegans are ciliated
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: 2020
year: '2020'
...
