---
_id: '15016'
abstract:
- lang: eng
text: 'The development, evolution, and function of the vertebrate central nervous
system (CNS) can be best studied using diverse model organisms. Amphibians, with
their unique phylogenetic position at the transition between aquatic and terrestrial
lifestyles, are valuable for understanding the origin and evolution of the tetrapod
brain and spinal cord. Their metamorphic developmental transitions and unique
regenerative abilities also facilitate the discovery of mechanisms for neural
circuit remodeling and replacement. The genetic toolkit for amphibians, however,
remains limited, with only a few species having sequenced genomes and a small
number of transgenic lines available. In mammals, recombinant adeno-associated
viral vectors (AAVs) have become a powerful alternative to genome modification
for visualizing and perturbing the nervous system. AAVs are DNA viruses that enable
neuronal transduction in both developing and adult animals with low toxicity and
spatial, temporal, and cell-type specificity. However, AAVs have never been shown
to transduce amphibian cells efficiently. To bridge this gap, we established a
simple, scalable, and robust strategy to screen AAV serotypes in three distantly-related
amphibian species: the frogs Xenopus laevis and Pelophylax bedriagae, and the
salamander Pleurodeles waltl, in both developing larval tadpoles and post-metamorphic
animals. For each species, we successfully identified at least two AAV serotypes
capable of infecting the CNS; however, no pan-amphibian serotype was identified,
indicating rapid evolution of AAV tropism. In addition, we developed an AAV-based
strategy that targets isochronic cohorts of developing neurons – a critical tool
for parsing neural circuit assembly. Finally, to enable visualization and manipulation
of neural circuits, we identified AAV variants for retrograde tracing of neuronal
projections in adult animals. Our findings expand the toolkit for amphibians to
include AAVs, establish a generalizable workflow for AAV screening in non-canonical
research organisms, generate testable hypotheses for the evolution of AAV tropism,
and lay the foundation for modern cross-species comparisons of vertebrate CNS
development, function, and evolution. '
acknowledgement: "We would like to extend our thanks to members of the Sweeney, Tosches,
Shein-Idelson,\r\nYamaguchi, Kelley, and Cline Labs for their contributions to this
project, discussion and support.\r\nWe additionally thank the Beckman Institute
Clover Center and Viviana Gradinaru (Caltech),\r\nKimberly Ritola (UNC NeuroTools),
Flavia Gama Gomez Leite (ISTA Viral Core), and Hüseyin\r\nCihan Önal (Shigemoto
Group, ISTA) for their consultation and assistance regarding AAVs, as\r\nwell as
Andras Simon and Alberto Joven for feedback and discussions on AAVs in Pleurodeles.\r\nTo
do these experiments, we have also benefited from the tremendous support of our
animal care and imaging facilities at our respective institutions, as well as the
amphibian stock centers\r\n(National Xenopus Resource Center, European Xenopus Resource
Center, Xenopus Express)\r\nand our funding sources: U.S. National Science Foundation
(NSF) Grant Number IOS 2110086\r\n(D.B.K., L.B.S., M.A.T., A.Y., and H.T.C.); United
States-Israel Binational Science Foundation\r\n(BSF) Grant Number 2020702 (M.S.-I.);
NSF Award Number 1645105 (G.J.G., M.E.H.); FTI\r\nStrategy Lower Austria Dissertation
Grant Number FTI21-D-046 (D.V.); Horizon Europe ERC\r\nStarting Grant Number 101041551
(L.B.S.); NIH grant number R35GM146973 (M.A.T.); Rita Allen\r\nFoundation award
number GA_032522_FE (M.A.T.); European Molecular Biology Organization\r\nLong-Term
Fellowship ALTF 874-2021 (A.D.); National Science Foundation Graduate Research\r\nFellowship
DGE 2036197 (E.C.J.B.); NIH grant number P40OD010997 (M.E.H)."
article_processing_charge: No
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. bioRxiv. doi:10.1101/2024.02.15.580289
apa: Jaeger, E. C. B., Vijatovic, D., Deryckere, A., Zorin, N., Nguyen, A. L., Ivanian,
G., … Sweeney, L. B. (n.d.). Adeno-associated viral tools to trace neural development
and connectivity across amphibians. bioRxiv. https://doi.org/10.1101/2024.02.15.580289
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.” BioRxiv,
n.d. https://doi.org/10.1101/2024.02.15.580289.
ieee: E. C. B. Jaeger et al., “Adeno-associated viral tools to trace neural
development and connectivity across amphibians,” bioRxiv. .
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. Adeno-associated viral tools to trace neural development and connectivity
across amphibians. bioRxiv, 10.1101/2024.02.15.580289.
mla: Jaeger, Eliza C. B., et al. “Adeno-Associated Viral Tools to Trace Neural Development
and Connectivity across Amphibians.” BioRxiv, doi:10.1101/2024.02.15.580289.
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, BioRxiv (n.d.).
date_created: 2024-02-20T09:20:32Z
date_published: 2024-02-16T00:00:00Z
date_updated: 2024-02-20T09:34:25Z
day: '16'
department:
- _id: LoSw
- _id: MaDe
- _id: GaNo
doi: 10.1101/2024.02.15.580289
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2024.02.15.580289
month: '02'
oa: 1
oa_version: Preprint
project:
- _id: bd73af52-d553-11ed-ba76-912049f0ac7a
grant_number: FTI21-D-046
name: Entwicklung und Funktion der V1 Interneuronen vom Schwimmen zum Laufen während
der Metamorphose von Xenopus
- _id: ebb66355-77a9-11ec-83b8-b8ac210a4dae
grant_number: '101041551'
name: Development and Evolution of Tetrapod Motor Circuits
publication: bioRxiv
publication_status: submitted
status: public
title: Adeno-associated viral tools to trace neural development and connectivity across
amphibians
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2024'
...
---
_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
- 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. eLife. 2022;11. doi:10.7554/eLife.68040
apa: Valperga, G., & de Bono, M. (2022). Impairing one sensory modality enhances
another by reconfiguring peptidergic signalling in Caenorhabditis elegans. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.68040
chicago: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances
Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” ELife.
eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.68040.
ieee: G. Valperga and M. de Bono, “Impairing one sensory modality enhances another
by reconfiguring peptidergic signalling in Caenorhabditis elegans,” eLife,
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.” ELife,
vol. 11, e68040, eLife Sciences Publications, 2022, doi:10.7554/eLife.68040.
short: G. Valperga, M. de Bono, ELife 11 (2022).
date_created: 2022-03-06T23:01:52Z
date_published: 2022-02-24T00:00:00Z
date_updated: 2023-08-02T14:42:55Z
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:
- 2050084X
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
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.
Autophagy. 2022;18(5):1208-1210. doi:10.1080/15548627.2022.2039523
apa: Artan, M., Sohn, J., Lee, C., Park, S. Y., & Lee, S. J. V. (2022). MON-2,
a Golgi protein, promotes longevity by upregulating autophagy through mediating
inter-organelle communications. Autophagy. Taylor & Francis. https://doi.org/10.1080/15548627.2022.2039523
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.” Autophagy. Taylor &
Francis, 2022. https://doi.org/10.1080/15548627.2022.2039523.
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,” Autophagy, vol. 18, no. 5. Taylor & 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.” Autophagy,
vol. 18, no. 5, Taylor & Francis, 2022, pp. 1208–10, doi:10.1080/15548627.2022.2039523.
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: 2023-10-03T10:54:54Z
day: '19'
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
- 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. Behavioral Neurogenetics. Vol 181.
NM. New York: Springer Nature; 2022:277-294. doi:10.1007/978-1-0716-2321-3_15'
apa: 'Artan, M., & de Bono, M. (2022). Proteomic Analysis of C. Elegans Neurons
Using TurboID-Based Proximity Labeling. In D. Yamamoto (Ed.), Behavioral Neurogenetics
(Vol. 181, pp. 277–294). New York: Springer Nature. https://doi.org/10.1007/978-1-0716-2321-3_15'
chicago: 'Artan, Murat, and Mario de Bono. “Proteomic Analysis of C. Elegans Neurons
Using TurboID-Based Proximity Labeling.” In Behavioral Neurogenetics, edited
by Daisuke Yamamoto, 181:277–94. NM. New York: Springer Nature, 2022. https://doi.org/10.1007/978-1-0716-2321-3_15.'
ieee: 'M. Artan and M. de Bono, “Proteomic Analysis of C. Elegans Neurons Using
TurboID-Based Proximity Labeling,” in Behavioral Neurogenetics, 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.” Behavioral Neurogenetics, edited
by Daisuke Yamamoto, vol. 181, Springer Nature, 2022, pp. 277–94, doi:10.1007/978-1-0716-2321-3_15.
short: M. Artan, M. de Bono, in:, D. Yamamoto (Ed.), Behavioral Neurogenetics, Springer
Nature, New York, 2022, pp. 277–294.
date_created: 2022-06-20T08:10:34Z
date_published: 2022-06-04T00:00:00Z
date_updated: 2023-02-21T09:51:55Z
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. PLoS Biology. 2022;20(6).
doi:10.1371/journal.pbio.3001684
apa: Zhao, L., Fenk, L. A., Nilsson, L., Amin-Wetzel, N. P., Ramirez, N., de Bono,
M., & Chen, C. (2022). ROS and cGMP signaling modulate persistent escape from
hypoxia in Caenorhabditis elegans. PLoS Biology. Public Library of Science.
https://doi.org/10.1371/journal.pbio.3001684
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.” PLoS Biology. Public Library
of Science, 2022. https://doi.org/10.1371/journal.pbio.3001684.
ieee: L. Zhao et al., “ROS and cGMP signaling modulate persistent escape
from hypoxia in Caenorhabditis elegans,” PLoS Biology, 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.” PLoS Biology, vol. 20, no. 6, e3001684,
Public Library of Science, 2022, doi:10.1371/journal.pbio.3001684.
short: L. Zhao, L.A. Fenk, L. Nilsson, N.P. Amin-Wetzel, N. Ramirez, M. de Bono,
C. Chen, PLoS Biology 20 (2022).
date_created: 2022-07-24T22:01:42Z
date_published: 2022-06-21T00:00:00Z
date_updated: 2023-08-03T12:11:44Z
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
- 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. Journal of Biological Chemistry. 2022;298(9). doi:10.1016/j.jbc.2022.102343
apa: 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. Elsevier.
https://doi.org/10.1016/j.jbc.2022.102343
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.” Journal of Biological Chemistry.
Elsevier, 2022. https://doi.org/10.1016/j.jbc.2022.102343.
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,” Journal of Biological Chemistry, 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.”
Journal of Biological Chemistry, vol. 298, no. 9, 102343, Elsevier, 2022,
doi:10.1016/j.jbc.2022.102343.
short: M. Artan, M. Hartl, W. Chen, M. de Bono, Journal of Biological Chemistry
298 (2022).
date_created: 2022-09-11T22:01:55Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2023-08-03T13:56:46Z
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. EMBO
Reports. 2022;23(7). doi:10.15252/embr.202154163
apa: Rahman, M., Ramirez, N., Diaz‐Balzac, C. A., & Bülow, H. E. (2022). Specific
N-glycans regulate an extracellular adhesion complex during somatosensory dendrite
patterning. EMBO Reports. Embo Press. https://doi.org/10.15252/embr.202154163
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.” EMBO Reports. Embo Press, 2022. https://doi.org/10.15252/embr.202154163.
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,”
EMBO Reports, 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.” EMBO Reports, vol. 23,
no. 7, e54163, Embo Press, 2022, doi:10.15252/embr.202154163.
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: 2023-10-03T11:25:54Z
day: '05'
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:10.5281/ZENODO.5519410
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. https://doi.org/10.5281/ZENODO.5519410
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. https://doi.org/10.5281/ZENODO.5519410.
ieee: L. Chauve et al., “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, 10.5281/ZENODO.5519410.
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.
Zenodo, 2021, doi:10.5281/ZENODO.5519410.
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: '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. eLife. 2021;10. doi:10.7554/eLife.68238
apa: Vuong-Brender, T., Flynn, S., Vallis, Y., & de Bono, M. (2021). Neuronal
calmodulin levels are controlled by CAMTA transcription factors. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.68238
chicago: Vuong-Brender, Thanh, Sean Flynn, Yvonne Vallis, and Mario de Bono. “Neuronal
Calmodulin Levels Are Controlled by CAMTA Transcription Factors.” ELife.
eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.68238.
ieee: T. Vuong-Brender, S. Flynn, Y. Vallis, and M. de Bono, “Neuronal calmodulin
levels are controlled by CAMTA transcription factors,” eLife, 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.” ELife, vol. 10, e68238, eLife Sciences Publications,
2021, doi:10.7554/eLife.68238.
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: 2023-08-14T07:23:39Z
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. Journal of Biological
Chemistry. 2021;297(3). doi:10.1016/J.JBC.2021.101094
apa: Artan, M., Barratt, S., Flynn, S. M., 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. Elsevier.
https://doi.org/10.1016/J.JBC.2021.101094
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.” Journal of Biological Chemistry.
Elsevier, 2021. https://doi.org/10.1016/J.JBC.2021.101094.
ieee: M. Artan et al., “Interactome analysis of Caenorhabditis elegans synapses
by TurboID-based proximity labeling,” Journal of Biological Chemistry,
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.” Journal of Biological Chemistry,
vol. 297, no. 3, 101094, Elsevier, 2021, doi:10.1016/J.JBC.2021.101094.
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: 2023-08-14T07:24:09Z
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. PLoS Biology. 2021;19(11). doi:10.1371/journal.pbio.3001431
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.
PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.3001431
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.” PLoS Biology. Public Library of Science,
2021. https://doi.org/10.1371/journal.pbio.3001431.
ieee: L. Chauve et al., “Neuronal HSF-1 coordinates the propagation of fat
desaturation across tissues to enable adaptation to high temperatures in C. elegans,”
PLoS Biology, 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.”
PLoS Biology, vol. 19, no. 11, e3001431, Public Library of Science, 2021,
doi:10.1371/journal.pbio.3001431.
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:
isi:
- '000715818400001'
pmid:
- '34723964'
file:
- access_level: open_access
checksum: 0c61b667f814fd9435b3ac42036fc36d
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-22T09:34:03Z
date_updated: 2021-11-22T09:34:03Z
file_id: '10330'
file_name: 2021_PLoSBio_Chauve.pdf
file_size: 4069215
relation: main_file
success: 1
file_date_updated: 2021-11-22T09:34:03Z
has_accepted_license: '1'
intvolume: ' 19'
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issue: '11'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Biology
publication_identifier:
eissn:
- 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: '7804'
abstract:
- lang: eng
text: Besides pro-inflammatory roles, the ancient cytokine interleukin-17 (IL-17)
modulates neural circuit function. We investigate IL-17 signaling in neurons,
and the extent it can alter organismal phenotypes. We combine immunoprecipitation
and mass spectrometry to biochemically characterize endogenous signaling complexes
that function downstream of IL-17 receptors in C. elegans neurons. We identify
the paracaspase MALT-1 as a critical output of the pathway. MALT1 mediates signaling
from many immune receptors in mammals, but was not previously implicated in IL-17
signaling or nervous system function. C. elegans MALT-1 forms a complex with homologs
of Act1 and IRAK and appears to function both as a scaffold and a protease. MALT-1
is expressed broadly in the C. elegans nervous system, and neuronal IL-17–MALT-1
signaling regulates multiple phenotypes, including escape behavior, associative
learning, immunity and longevity. Our data suggest MALT1 has an ancient role modulating
neural circuit function downstream of IL-17 to remodel physiology and behavior.
article_number: '2099'
article_processing_charge: No
article_type: original
author:
- first_name: Sean M.
full_name: Flynn, Sean M.
last_name: Flynn
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- 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
last_name: Barratt
- first_name: Alastair
full_name: Crisp, Alastair
last_name: Crisp
- first_name: Geoffrey M.
full_name: Nelson, Geoffrey M.
last_name: Nelson
- first_name: Sew Yeu
full_name: Peak-Chew, Sew Yeu
last_name: Peak-Chew
- first_name: Farida
full_name: Begum, Farida
last_name: Begum
- first_name: Mark
full_name: Skehel, Mark
last_name: Skehel
- 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: Flynn SM, Chen C, Artan M, et al. MALT-1 mediates IL-17 neural signaling to
regulate C. elegans behavior, immunity and longevity. Nature Communications.
2020;11. doi:10.1038/s41467-020-15872-y
apa: Flynn, S. M., Chen, C., Artan, M., Barratt, S., Crisp, A., Nelson, G. M., …
de Bono, M. (2020). MALT-1 mediates IL-17 neural signaling to regulate C. elegans
behavior, immunity and longevity. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-020-15872-y
chicago: Flynn, Sean M., Changchun Chen, Murat Artan, Stephen Barratt, Alastair
Crisp, Geoffrey M. Nelson, Sew Yeu Peak-Chew, Farida Begum, Mark Skehel, and Mario
de Bono. “MALT-1 Mediates IL-17 Neural Signaling to Regulate C. Elegans Behavior,
Immunity and Longevity.” Nature Communications. Springer Nature, 2020.
https://doi.org/10.1038/s41467-020-15872-y.
ieee: S. M. Flynn et al., “MALT-1 mediates IL-17 neural signaling to regulate C.
elegans behavior, immunity and longevity,” Nature Communications, vol.
11. Springer Nature, 2020.
ista: Flynn SM, Chen C, Artan M, Barratt S, Crisp A, Nelson GM, Peak-Chew SY, Begum
F, Skehel M, de Bono M. 2020. MALT-1 mediates IL-17 neural signaling to regulate C.
elegans behavior, immunity and longevity. Nature Communications. 11, 2099.
mla: Flynn, Sean M., et al. “MALT-1 Mediates IL-17 Neural Signaling to Regulate C.
Elegans Behavior, Immunity and Longevity.” Nature Communications, vol.
11, 2099, Springer Nature, 2020, doi:10.1038/s41467-020-15872-y.
short: S.M. Flynn, C. Chen, M. Artan, S. Barratt, A. Crisp, G.M. Nelson, S.Y. Peak-Chew,
F. Begum, M. Skehel, M. de Bono, Nature Communications 11 (2020).
date_created: 2020-05-10T22:00:47Z
date_published: 2020-04-29T00:00:00Z
date_updated: 2023-08-21T06:21:14Z
day: '29'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1038/s41467-020-15872-y
external_id:
isi:
- '000531855500029'
file:
- access_level: open_access
checksum: dce367abf2c1a1d15f58fe6f7de82893
content_type: application/pdf
creator: dernst
date_created: 2020-05-11T10:36:33Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7817'
file_name: 2020_NatureComm_Flynn.pdf
file_size: 4609120
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity
and longevity
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: 11
year: '2020'
...
---
_id: '7546'
abstract:
- lang: eng
text: The extent to which behavior is shaped by experience varies between individuals.
Genetic differences contribute to this variation, but the neural mechanisms are
not understood. Here, we dissect natural variation in the behavioral flexibility
of two Caenorhabditis elegans wild strains. In one strain, a memory of exposure
to 21% O2 suppresses CO2-evoked locomotory arousal; in the other, CO2 evokes arousal
regardless of previous O2 experience. We map that variation to a polymorphic dendritic
scaffold protein, ARCP-1, expressed in sensory neurons. ARCP-1 binds the Ca2+-dependent
phosphodiesterase PDE-1 and co-localizes PDE-1 with molecular sensors for CO2
at dendritic ends. Reducing ARCP-1 or PDE-1 activity promotes CO2 escape by altering
neuropeptide expression in the BAG CO2 sensors. Variation in ARCP-1 alters behavioral
plasticity in multiple paradigms. Our findings are reminiscent of genetic accommodation,
an evolutionary process by which phenotypic flexibility in response to environmental
variation is reset by genetic change.
article_processing_charge: No
article_type: original
author:
- first_name: Isabel
full_name: Beets, Isabel
last_name: Beets
- first_name: Gaotian
full_name: Zhang, Gaotian
last_name: Zhang
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Geoffrey M.
full_name: Nelson, Geoffrey M.
last_name: Nelson
- first_name: Marie-Anne
full_name: Félix, Marie-Anne
last_name: Félix
- 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: Beets I, Zhang G, Fenk LA, et al. Natural variation in a dendritic scaffold
protein remodels experience-dependent plasticity by altering neuropeptide expression.
Neuron. 2020;105(1):106-121.e10. doi:10.1016/j.neuron.2019.10.001
apa: Beets, I., Zhang, G., Fenk, L. A., Chen, C., Nelson, G. M., Félix, M.-A., &
de Bono, M. (2020). Natural variation in a dendritic scaffold protein remodels
experience-dependent plasticity by altering neuropeptide expression. Neuron.
Cell Press. https://doi.org/10.1016/j.neuron.2019.10.001
chicago: Beets, Isabel, Gaotian Zhang, Lorenz A. Fenk, Changchun Chen, Geoffrey
M. Nelson, Marie-Anne Félix, and Mario de Bono. “Natural Variation in a Dendritic
Scaffold Protein Remodels Experience-Dependent Plasticity by Altering Neuropeptide
Expression.” Neuron. Cell Press, 2020. https://doi.org/10.1016/j.neuron.2019.10.001.
ieee: I. Beets et al., “Natural variation in a dendritic scaffold protein
remodels experience-dependent plasticity by altering neuropeptide expression,”
Neuron, vol. 105, no. 1. Cell Press, p. 106–121.e10, 2020.
ista: Beets I, Zhang G, Fenk LA, Chen C, Nelson GM, Félix M-A, de Bono M. 2020.
Natural variation in a dendritic scaffold protein remodels experience-dependent
plasticity by altering neuropeptide expression. Neuron. 105(1), 106–121.e10.
mla: Beets, Isabel, et al. “Natural Variation in a Dendritic Scaffold Protein Remodels
Experience-Dependent Plasticity by Altering Neuropeptide Expression.” Neuron,
vol. 105, no. 1, Cell Press, 2020, p. 106–121.e10, doi:10.1016/j.neuron.2019.10.001.
short: I. Beets, G. Zhang, L.A. Fenk, C. Chen, G.M. Nelson, M.-A. Félix, M. de Bono,
Neuron 105 (2020) 106–121.e10.
date_created: 2020-02-28T10:43:39Z
date_published: 2020-01-08T00:00:00Z
date_updated: 2023-08-18T06:46:23Z
day: '08'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1016/j.neuron.2019.10.001
external_id:
isi:
- '000507341300012'
pmid:
- '31757604'
file:
- access_level: open_access
checksum: 799bfd297a008753a688b30d3958fa48
content_type: application/pdf
creator: dernst
date_created: 2020-03-02T15:43:57Z
date_updated: 2020-07-14T12:48:00Z
file_id: '7558'
file_name: 2020_Neuron_Beets.pdf
file_size: 3294066
relation: main_file
file_date_updated: 2020-07-14T12:48:00Z
has_accepted_license: '1'
intvolume: ' 105'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 106-121.e10
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Cell Press
quality_controlled: '1'
status: public
title: Natural variation in a dendritic scaffold protein remodels experience-dependent
plasticity by altering neuropeptide expression
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: 105
year: '2020'
...
---
_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. Science Advances. 2020;6(27). doi:10.1126/sciadv.aaw7824
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.
Science Advances. American Association for the Advancement of Science.
https://doi.org/10.1126/sciadv.aaw7824
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.” Science Advances.
American Association for the Advancement of Science, 2020. https://doi.org/10.1126/sciadv.aaw7824.
ieee: S. Park et al., “VRK-1 extends life span by activation of AMPK via
phosphorylation,” Science Advances, 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.”
Science Advances, vol. 6, no. 27, aaw7824, American Association for the
Advancement of Science, 2020, doi:10.1126/sciadv.aaw7824.
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'
...
---
_id: '7340'
abstract:
- lang: eng
text: Coupling of endoplasmic reticulum stress to dimerisation‑dependent activation
of the UPR transducer IRE1 is incompletely understood. Whilst the luminal co-chaperone
ERdj4 promotes a complex between the Hsp70 BiP and IRE1's stress-sensing luminal
domain (IRE1LD) that favours the latter's monomeric inactive state and loss of
ERdj4 de-represses IRE1, evidence linking these cellular and in vitro observations
is presently lacking. We report that enforced loading of endogenous BiP onto endogenous
IRE1α repressed UPR signalling in CHO cells and deletions in the IRE1α locus that
de-repressed the UPR in cells, encode flexible regions of IRE1LD that mediated
BiP‑induced monomerisation in vitro. Changes in the hydrogen exchange mass spectrometry
profile of IRE1LD induced by ERdj4 and BiP confirmed monomerisation and were consistent
with active destabilisation of the IRE1LD dimer. Together, these observations
support a competition model whereby waning ER stress passively partitions ERdj4
and BiP to IRE1LD to initiate active repression of UPR signalling.
acknowledgement: We thank the CIMR flow cytometry core facility team (Reiner Schulte,
Chiara Cossetti and Gabriela Grondys-Kotarba) for assistance with FACS, the Huntington
lab for access to the Octet machine, Steffen Preissler for advice on data interpretation,
Roman Kityk and Nicole Luebbehusen for help and advice with HX-MS experiments.
article_number: e50793
article_processing_charge: No
article_type: original
author:
- first_name: Niko Paresh
full_name: Amin-Wetzel, Niko Paresh
id: E95D3014-9D8C-11E9-9C80-D2F8E5697425
last_name: Amin-Wetzel
- first_name: Lisa
full_name: Neidhardt, Lisa
last_name: Neidhardt
- first_name: Yahui
full_name: Yan, Yahui
last_name: Yan
- first_name: Matthias P.
full_name: Mayer, Matthias P.
last_name: Mayer
- first_name: David
full_name: Ron, David
last_name: Ron
citation:
ama: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. Unstructured regions in
IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression
of the UPR. eLife. 2019;8. doi:10.7554/eLife.50793
apa: Amin-Wetzel, N. P., Neidhardt, L., Yan, Y., Mayer, M. P., & Ron, D. (2019).
Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal
domain dimer and repression of the UPR. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.50793
chicago: Amin-Wetzel, Niko Paresh, Lisa Neidhardt, Yahui Yan, Matthias P. Mayer,
and David Ron. “Unstructured Regions in IRE1α Specify BiP-Mediated Destabilisation
of the Luminal Domain Dimer and Repression of the UPR.” ELife. eLife Sciences
Publications, 2019. https://doi.org/10.7554/eLife.50793.
ieee: N. P. Amin-Wetzel, L. Neidhardt, Y. Yan, M. P. Mayer, and D. Ron, “Unstructured
regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer
and repression of the UPR,” eLife, vol. 8. eLife Sciences Publications,
2019.
ista: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. 2019. Unstructured regions
in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and
repression of the UPR. eLife. 8, e50793.
mla: Amin-Wetzel, Niko Paresh, et al. “Unstructured Regions in IRE1α Specify BiP-Mediated
Destabilisation of the Luminal Domain Dimer and Repression of the UPR.” ELife,
vol. 8, e50793, eLife Sciences Publications, 2019, doi:10.7554/eLife.50793.
short: N.P. Amin-Wetzel, L. Neidhardt, Y. Yan, M.P. Mayer, D. Ron, ELife 8 (2019).
date_created: 2020-01-19T23:00:39Z
date_published: 2019-12-24T00:00:00Z
date_updated: 2023-09-06T14:58:02Z
day: '24'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.7554/eLife.50793
external_id:
isi:
- '000512303700001'
pmid:
- '31873072'
file:
- access_level: open_access
checksum: 29fcbcd8c1fc7f11a596ed7f14ea1c82
content_type: application/pdf
creator: dernst
date_created: 2020-11-19T11:37:41Z
date_updated: 2020-11-19T11:37:41Z
file_id: '8777'
file_name: 2019_eLife_AminWetzel.pdf
file_size: 4817384
relation: main_file
success: 1
file_date_updated: 2020-11-19T11:37:41Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal
domain dimer and repression of the UPR
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2019'
...