---
_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
license: https://creativecommons.org/licenses/by/4.0/
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: '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: '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'
isi: 1
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: '7545'
abstract:
- lang: eng
text: Neuronal activity often leads to alterations in gene expression and cellular
architecture. The nematode Caenorhabditis elegans, owing to its compact translucent
nervous system, is a powerful system in which to study conserved aspects of the
development and plasticity of neuronal morphology. Here we focus on one pair of
sensory neurons, termed URX, which the worm uses to sense and avoid high levels
of environmental oxygen. Previous studies have reported that the URX neuron pair
has variable branched endings at its dendritic sensory tip. By controlling oxygen
levels and analyzing mutants, we found that these microtubule-rich branched endings
grow over time as a consequence of neuronal activity in adulthood. We also find
that the growth of these branches correlates with an increase in cellular sensitivity
to particular ranges of oxygen that is observable in the behavior of older worms.
Given the strengths of C. elegans as a model organism, URX may serve as a potent
system for uncovering genes and mechanisms involved in activity-dependent morphological
changes in neurons and possible adaptive changes in the aging nervous system.
article_processing_charge: No
article_type: original
author:
- first_name: Jesse A.
full_name: Cohn, Jesse A.
last_name: Cohn
- first_name: Elizabeth R.
full_name: Cebul, Elizabeth R.
last_name: Cebul
- first_name: Giulio
full_name: Valperga, Giulio
last_name: Valperga
- first_name: Lotti
full_name: Brose, Lotti
last_name: Brose
- 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: Maxwell G.
full_name: Heiman, Maxwell G.
last_name: Heiman
- first_name: Jonathan T.
full_name: Pierce, Jonathan T.
last_name: Pierce
citation:
ama: Cohn JA, Cebul ER, Valperga G, et al. Long-term activity drives dendritic branch
elaboration of a C. elegans sensory neuron. Developmental Biology. 2020;461(1):66-74.
doi:10.1016/j.ydbio.2020.01.005
apa: Cohn, J. A., Cebul, E. R., Valperga, G., Brose, L., de Bono, M., Heiman, M.
G., & Pierce, J. T. (2020). Long-term activity drives dendritic branch elaboration
of a C. elegans sensory neuron. Developmental Biology. Elsevier. https://doi.org/10.1016/j.ydbio.2020.01.005
chicago: Cohn, Jesse A., Elizabeth R. Cebul, Giulio Valperga, Lotti Brose, Mario
de Bono, Maxwell G. Heiman, and Jonathan T. Pierce. “Long-Term Activity Drives
Dendritic Branch Elaboration of a C. Elegans Sensory Neuron.” Developmental
Biology. Elsevier, 2020. https://doi.org/10.1016/j.ydbio.2020.01.005.
ieee: J. A. Cohn et al., “Long-term activity drives dendritic branch elaboration
of a C. elegans sensory neuron,” Developmental Biology, vol. 461, no. 1.
Elsevier, pp. 66–74, 2020.
ista: Cohn JA, Cebul ER, Valperga G, Brose L, de Bono M, Heiman MG, Pierce JT. 2020.
Long-term activity drives dendritic branch elaboration of a C. elegans sensory
neuron. Developmental Biology. 461(1), 66–74.
mla: Cohn, Jesse A., et al. “Long-Term Activity Drives Dendritic Branch Elaboration
of a C. Elegans Sensory Neuron.” Developmental Biology, vol. 461, no. 1,
Elsevier, 2020, pp. 66–74, doi:10.1016/j.ydbio.2020.01.005.
short: J.A. Cohn, E.R. Cebul, G. Valperga, L. Brose, M. de Bono, M.G. Heiman, J.T.
Pierce, Developmental Biology 461 (2020) 66–74.
date_created: 2020-02-28T10:38:32Z
date_published: 2020-05-01T00:00:00Z
date_updated: 2021-01-12T08:14:06Z
day: '01'
doi: 10.1016/j.ydbio.2020.01.005
extern: '1'
intvolume: ' 461'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/685339
month: '05'
oa: 1
oa_version: Preprint
page: 66-74
publication: Developmental Biology
publication_identifier:
issn:
- 0012-1606
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Long-term activity drives dendritic branch elaboration of a C. elegans sensory
neuron
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 461
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: '7547'
abstract:
- lang: eng
text: The BH3-only family of proteins is key for initiating apoptosis in a variety
of contexts, and may also contribute to non-apoptotic cellular processes. Historically,
the nematode Caenorhabditis elegans has provided a powerful system for studying
and identifying conserved regulators of BH3-only proteins. In C. elegans, the
BH3-only protein egl-1 is expressed during development to cell-autonomously trigger
most developmental cell deaths. Here we provide evidence that egl-1 is also transcribed
after development in the sensory neuron pair URX without inducing apoptosis. We
used genetic screening and epistasis analysis to determine that its transcription
is regulated in URX by neuronal activity and/or in parallel by orthologs of Protein
Kinase G and the Salt-Inducible Kinase family. Because several BH3-only family
proteins are also expressed in the adult nervous system of mammals, we suggest
that studying egl-1 expression in URX may shed light on mechanisms that regulate
conserved family members in higher organisms.
article_processing_charge: No
article_type: original
author:
- first_name: Jesse
full_name: Cohn, Jesse
last_name: Cohn
- first_name: Vivek
full_name: Dwivedi, Vivek
last_name: Dwivedi
- first_name: Giulio
full_name: Valperga, Giulio
last_name: Valperga
- first_name: Nicole
full_name: Zarate, Nicole
last_name: Zarate
- 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: H. Robert
full_name: Horvitz, H. Robert
last_name: Horvitz
- first_name: Jonathan T.
full_name: Pierce, Jonathan T.
last_name: Pierce
citation:
ama: 'Cohn J, Dwivedi V, Valperga G, et al. Activity-dependent regulation of the
proapoptotic BH3-only gene egl-1 in a living neuron pair in Caenorhabditis elegans.
G3: Genes, Genomes, Genetics. 2019;9(11):3703-3714. doi:10.1534/g3.119.400654'
apa: 'Cohn, J., Dwivedi, V., Valperga, G., Zarate, N., de Bono, M., Horvitz, H.
R., & Pierce, J. T. (2019). Activity-dependent regulation of the proapoptotic
BH3-only gene egl-1 in a living neuron pair in Caenorhabditis elegans. G3:
Genes, Genomes, Genetics. Genetics Society of America. https://doi.org/10.1534/g3.119.400654'
chicago: 'Cohn, Jesse, Vivek Dwivedi, Giulio Valperga, Nicole Zarate, Mario de Bono,
H. Robert Horvitz, and Jonathan T. Pierce. “Activity-Dependent Regulation of the
Proapoptotic BH3-Only Gene Egl-1 in a Living Neuron Pair in Caenorhabditis Elegans.”
G3: Genes, Genomes, Genetics. Genetics Society of America, 2019. https://doi.org/10.1534/g3.119.400654.'
ieee: 'J. Cohn et al., “Activity-dependent regulation of the proapoptotic
BH3-only gene egl-1 in a living neuron pair in Caenorhabditis elegans,” G3:
Genes, Genomes, Genetics, vol. 9, no. 11. Genetics Society of America, pp.
3703–3714, 2019.'
ista: 'Cohn J, Dwivedi V, Valperga G, Zarate N, de Bono M, Horvitz HR, Pierce JT.
2019. Activity-dependent regulation of the proapoptotic BH3-only gene egl-1 in
a living neuron pair in Caenorhabditis elegans. G3: Genes, Genomes, Genetics.
9(11), 3703–3714.'
mla: 'Cohn, Jesse, et al. “Activity-Dependent Regulation of the Proapoptotic BH3-Only
Gene Egl-1 in a Living Neuron Pair in Caenorhabditis Elegans.” G3: Genes, Genomes,
Genetics, vol. 9, no. 11, Genetics Society of America, 2019, pp. 3703–14,
doi:10.1534/g3.119.400654.'
short: 'J. Cohn, V. Dwivedi, G. Valperga, N. Zarate, M. de Bono, H.R. Horvitz, J.T.
Pierce, G3: Genes, Genomes, Genetics 9 (2019) 3703–3714.'
date_created: 2020-02-28T10:44:27Z
date_published: 2019-11-01T00:00:00Z
date_updated: 2021-01-12T08:14:07Z
day: '01'
doi: 10.1534/g3.119.400654
extern: '1'
external_id:
pmid:
- '31519744'
intvolume: ' 9'
issue: '11'
language:
- iso: eng
month: '11'
oa_version: Published Version
page: 3703-3714
pmid: 1
publication: 'G3: Genes, Genomes, Genetics'
publication_identifier:
issn:
- 2160-1836
publication_status: published
publisher: Genetics Society of America
quality_controlled: '1'
status: public
title: Activity-dependent regulation of the proapoptotic BH3-only gene egl-1 in a
living neuron pair in Caenorhabditis elegans
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2019'
...
---
_id: '7548'
abstract:
- lang: eng
text: Although the aggregation of the amyloid-β peptide (Aβ) into amyloid fibrils
is a well-established hallmark of Alzheimer’s disease, the complex mechanisms
linking this process to neurodegeneration are still incompletely understood. The
nematode worm C. elegans is a valuable model organism through which to study these
mechanisms because of its simple nervous system and its relatively short lifespan.
Standard Aβ-based C. elegans models of Alzheimer’s disease are designed to study
the toxic effects of the overexpression of Aβ in the muscle or nervous systems.
However, the wide variety of effects associated with the tissue-level overexpression
of Aβ makes it difficult to single out and study specific cellular mechanisms
related to the onset of Alzheimer’s disease. Here, to better understand how to
investigate the early events affecting neuronal signalling, we created a C. elegans
model expressing Aβ42, the 42-residue form of Aβ, from a single-copy gene insertion
in just one pair of glutamatergic sensory neurons, the BAG neurons. In behavioural
assays, we found that the Aβ42-expressing animals displayed a subtle modulation
of the response to CO2, compared to controls. Ca2+ imaging revealed that the BAG
neurons in young Aβ42-expressing nematodes were activated more strongly than in
control animals, and that neuronal activation remained intact until old age. Taken
together, our results suggest that Aβ42-expression in this very subtle model of
AD is sufficient to modulate the behavioural response but not strong enough to
generate significant neurotoxicity, suggesting that slightly more aggressive perturbations
will enable effectively studies of the links between the modulation of a physiological
response and its associated neurotoxicity.
article_number: e0217746
article_processing_charge: No
article_type: original
author:
- first_name: Tessa
full_name: Sinnige, Tessa
last_name: Sinnige
- first_name: Prashanth
full_name: Ciryam, Prashanth
last_name: Ciryam
- first_name: Samuel
full_name: Casford, Samuel
last_name: Casford
- first_name: Christopher M.
full_name: Dobson, Christopher M.
last_name: Dobson
- 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: Michele
full_name: Vendruscolo, Michele
last_name: Vendruscolo
citation:
ama: Sinnige T, Ciryam P, Casford S, Dobson CM, de Bono M, Vendruscolo M. Expression
of the amyloid-β peptide in a single pair of C. elegans sensory neurons modulates
the associated behavioural response. PLOS ONE. 2019;14(5). doi:10.1371/journal.pone.0217746
apa: Sinnige, T., Ciryam, P., Casford, S., Dobson, C. M., de Bono, M., & Vendruscolo,
M. (2019). Expression of the amyloid-β peptide in a single pair of C. elegans
sensory neurons modulates the associated behavioural response. PLOS ONE.
Public Library of Science. https://doi.org/10.1371/journal.pone.0217746
chicago: Sinnige, Tessa, Prashanth Ciryam, Samuel Casford, Christopher M. Dobson,
Mario de Bono, and Michele Vendruscolo. “Expression of the Amyloid-β Peptide in
a Single Pair of C. Elegans Sensory Neurons Modulates the Associated Behavioural
Response.” PLOS ONE. Public Library of Science, 2019. https://doi.org/10.1371/journal.pone.0217746.
ieee: T. Sinnige, P. Ciryam, S. Casford, C. M. Dobson, M. de Bono, and M. Vendruscolo,
“Expression of the amyloid-β peptide in a single pair of C. elegans sensory neurons
modulates the associated behavioural response,” PLOS ONE, vol. 14, no.
5. Public Library of Science, 2019.
ista: Sinnige T, Ciryam P, Casford S, Dobson CM, de Bono M, Vendruscolo M. 2019.
Expression of the amyloid-β peptide in a single pair of C. elegans sensory neurons
modulates the associated behavioural response. PLOS ONE. 14(5), e0217746.
mla: Sinnige, Tessa, et al. “Expression of the Amyloid-β Peptide in a Single Pair
of C. Elegans Sensory Neurons Modulates the Associated Behavioural Response.”
PLOS ONE, vol. 14, no. 5, e0217746, Public Library of Science, 2019, doi:10.1371/journal.pone.0217746.
short: T. Sinnige, P. Ciryam, S. Casford, C.M. Dobson, M. de Bono, M. Vendruscolo,
PLOS ONE 14 (2019).
date_created: 2020-02-28T10:45:13Z
date_published: 2019-05-31T00:00:00Z
date_updated: 2021-01-12T08:14:08Z
day: '31'
doi: 10.1371/journal.pone.0217746
extern: '1'
intvolume: ' 14'
issue: '5'
language:
- iso: eng
month: '05'
oa_version: Published Version
publication: PLOS ONE
publication_identifier:
issn:
- 1932-6203
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: Expression of the amyloid-β peptide in a single pair of C. elegans sensory
neurons modulates the associated behavioural response
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2019'
...
---
_id: '6109'
abstract:
- lang: eng
text: Neuropeptides are ubiquitous modulators of behavior and physiology. They are
packaged in specialized secretory organelles called dense core vesicles (DCVs)
that are released upon neural stimulation. Unlike synaptic vesicles, which can
be recycled and refilled close to release sites, DCVs must be replenished by de
novo synthesis in the cell body. Here, we dissect DCV cell biology in vivo in
a Caenorhabditis elegans sensory neuron whose tonic activity we can control using
a natural stimulus. We express fluorescently tagged neuropeptides in the neuron
and define parameters that describe their subcellular distribution. We measure
these parameters at high and low neural activity in 187 mutants defective in proteins
implicated in membrane traffic, neuroendocrine secretion, and neuronal or synaptic
activity. Using unsupervised hierarchical clustering methods, we analyze these
data and identify 62 groups of genes with similar mutant phenotypes. We explore
the function of a subset of these groups. We recapitulate many previous findings,
validating our paradigm. We uncover a large battery of proteins involved in recycling
DCV membrane proteins, something hitherto poorly explored. We show that the unfolded
protein response promotes DCV production, which may contribute to intertissue
communication of stress. We also find evidence that different mechanisms of priming
and exocytosis may operate at high and low neural activity. Our work provides
a defined framework to study DCV biology at different neural activity levels.
author:
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
- first_name: QueeLim
full_name: Ch’ng, QueeLim
last_name: Ch’ng
- first_name: Maëlle
full_name: Jospin, Maëlle
last_name: Jospin
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Ramiro
full_name: Lorenzo, Ramiro
last_name: Lorenzo
- 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: Laurent P, Ch’ng Q, Jospin M, Chen C, Lorenzo R, de Bono M. Genetic dissection
of neuropeptide cell biology at high and low activity in a defined sensory neuron.
Proceedings of the National Academy of Sciences. 2018;115(29):E6890-E6899.
doi:10.1073/pnas.1714610115
apa: Laurent, P., Ch’ng, Q., Jospin, M., Chen, C., Lorenzo, R., & de Bono, M.
(2018). Genetic dissection of neuropeptide cell biology at high and low activity
in a defined sensory neuron. Proceedings of the National Academy of Sciences.
National Academy of Sciences. https://doi.org/10.1073/pnas.1714610115
chicago: Laurent, Patrick, QueeLim Ch’ng, Maëlle Jospin, Changchun Chen, Ramiro
Lorenzo, and Mario de Bono. “Genetic Dissection of Neuropeptide Cell Biology at
High and Low Activity in a Defined Sensory Neuron.” Proceedings of the National
Academy of Sciences. National Academy of Sciences, 2018. https://doi.org/10.1073/pnas.1714610115.
ieee: P. Laurent, Q. Ch’ng, M. Jospin, C. Chen, R. Lorenzo, and M. de Bono, “Genetic
dissection of neuropeptide cell biology at high and low activity in a defined
sensory neuron,” Proceedings of the National Academy of Sciences, vol.
115, no. 29. National Academy of Sciences, pp. E6890–E6899, 2018.
ista: Laurent P, Ch’ng Q, Jospin M, Chen C, Lorenzo R, de Bono M. 2018. Genetic
dissection of neuropeptide cell biology at high and low activity in a defined
sensory neuron. Proceedings of the National Academy of Sciences. 115(29), E6890–E6899.
mla: Laurent, Patrick, et al. “Genetic Dissection of Neuropeptide Cell Biology at
High and Low Activity in a Defined Sensory Neuron.” Proceedings of the National
Academy of Sciences, vol. 115, no. 29, National Academy of Sciences, 2018,
pp. E6890–99, doi:10.1073/pnas.1714610115.
short: P. Laurent, Q. Ch’ng, M. Jospin, C. Chen, R. Lorenzo, M. de Bono, Proceedings
of the National Academy of Sciences 115 (2018) E6890–E6899.
date_created: 2019-03-19T12:41:33Z
date_published: 2018-07-17T00:00:00Z
date_updated: 2021-01-12T08:06:09Z
day: '17'
ddc:
- '570'
doi: 10.1073/pnas.1714610115
extern: '1'
external_id:
pmid:
- '29959203'
file:
- access_level: open_access
checksum: 5e81665377441cdd8d99ab952c534319
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T13:01:58Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6110'
file_name: 2018_PNAS_Laurent.pdf
file_size: 1567765
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 115'
issue: '29'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '07'
oa: 1
oa_version: Published Version
page: E6890-E6899
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
issn:
- 0027-8424
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
status: public
title: Genetic dissection of neuropeptide cell biology at high and low activity in
a defined sensory neuron
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 115
year: '2018'
...
---
_id: '6111'
abstract:
- lang: eng
text: 'Neurons develop elaborate morphologies that provide a model for understanding
cellular architecture. By studying C. elegans sensory dendrites, we previously
identified genes that act to promote the extension of ciliated sensory dendrites
during embryogenesis. Interestingly, the nonciliated dendrite of the oxygen-sensing
neuron URX is not affected by these genes, suggesting it develops through a distinct
mechanism. Here, we use a visual forward genetic screen to identify mutants that
affect URX dendrite morphogenesis. We find that disruption of the MAP kinase MAPK-15
or the βH-spectrin SMA-1 causes a phenotype opposite to what we had seen before:
dendrites extend normally during embryogenesis but begin to overgrow as the animals
reach adulthood, ultimately extending up to 150% of their normal length. SMA-1
is broadly expressed and acts non-cell-autonomously, while MAPK-15 is expressed
in many sensory neurons including URX and acts cell-autonomously. MAPK-15 acts
at the time of overgrowth, localizes at the dendrite ending, and requires its
kinase activity, suggesting it acts locally in time and space to constrain dendrite
growth. Finally, we find that the oxygen-sensing guanylate cyclase GCY-35, which
normally localizes at the dendrite ending, is localized throughout the overgrown
region, and that overgrowth can be suppressed by overexpressing GCY-35 or by genetically
mimicking elevated cGMP signaling. These results suggest that overgrowth may correspond
to expansion of a sensory compartment at the dendrite ending, reminiscent of the
remodeling of sensory cilia or dendritic spines. Thus, in contrast to established
pathways that promote dendrite growth during early development, our results reveal
a distinct mechanism that constrains dendrite growth throughout the life of the
animal, possibly by controlling the size of a sensory compartment at the dendrite
ending.'
article_number: e1007435
author:
- first_name: Ian G.
full_name: McLachlan, Ian G.
last_name: McLachlan
- first_name: Isabel
full_name: Beets, Isabel
last_name: Beets
- 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: Maxwell G.
full_name: Heiman, Maxwell G.
last_name: Heiman
citation:
ama: McLachlan IG, Beets I, de Bono M, Heiman MG. A neuronal MAP kinase constrains
growth of a Caenorhabditis elegans sensory dendrite throughout the life of the
organism. PLOS Genetics. 2018;14(6). doi:10.1371/journal.pgen.1007435
apa: McLachlan, I. G., Beets, I., de Bono, M., & Heiman, M. G. (2018). A neuronal
MAP kinase constrains growth of a Caenorhabditis elegans sensory dendrite throughout
the life of the organism. PLOS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007435
chicago: McLachlan, Ian G., Isabel Beets, Mario de Bono, and Maxwell G. Heiman.
“A Neuronal MAP Kinase Constrains Growth of a Caenorhabditis Elegans Sensory Dendrite
throughout the Life of the Organism.” PLOS Genetics. Public Library of
Science, 2018. https://doi.org/10.1371/journal.pgen.1007435.
ieee: I. G. McLachlan, I. Beets, M. de Bono, and M. G. Heiman, “A neuronal MAP kinase
constrains growth of a Caenorhabditis elegans sensory dendrite throughout the
life of the organism,” PLOS Genetics, vol. 14, no. 6. Public Library of
Science, 2018.
ista: McLachlan IG, Beets I, de Bono M, Heiman MG. 2018. A neuronal MAP kinase constrains
growth of a Caenorhabditis elegans sensory dendrite throughout the life of the
organism. PLOS Genetics. 14(6), e1007435.
mla: McLachlan, Ian G., et al. “A Neuronal MAP Kinase Constrains Growth of a Caenorhabditis
Elegans Sensory Dendrite throughout the Life of the Organism.” PLOS Genetics,
vol. 14, no. 6, e1007435, Public Library of Science, 2018, doi:10.1371/journal.pgen.1007435.
short: I.G. McLachlan, I. Beets, M. de Bono, M.G. Heiman, PLOS Genetics 14 (2018).
date_created: 2019-03-19T13:09:28Z
date_published: 2018-06-07T00:00:00Z
date_updated: 2021-01-12T08:06:11Z
day: '07'
ddc:
- '570'
doi: 10.1371/journal.pgen.1007435
extern: '1'
external_id:
pmid:
- '29879119'
file:
- access_level: open_access
checksum: 622036b945365dbc575bea2768aa9bc8
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T13:18:01Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6112'
file_name: 2018_PLOS_McLachlan.pdf
file_size: 13011506
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: A neuronal MAP kinase constrains growth of a Caenorhabditis elegans sensory
dendrite throughout the life of the organism
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2018'
...
---
_id: '6113'
author:
- first_name: Shigekazu
full_name: Oda, Shigekazu
last_name: Oda
- first_name: Yu
full_name: Toyoshima, Yu
last_name: Toyoshima
- 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: Oda S, Toyoshima Y, de Bono M. Modulation of sensory information processing
by a neuroglobin in Caenorhabditis elegans. Proceedings of the National Academy
of Sciences. 2017;114(23):E4658-E4665. doi:10.1073/pnas.1614596114
apa: Oda, S., Toyoshima, Y., & de Bono, M. (2017). Modulation of sensory information
processing by a neuroglobin in Caenorhabditis elegans. Proceedings of the National
Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1614596114
chicago: Oda, Shigekazu, Yu Toyoshima, and Mario de Bono. “Modulation of Sensory
Information Processing by a Neuroglobin in Caenorhabditis Elegans.” Proceedings
of the National Academy of Sciences. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1614596114.
ieee: S. Oda, Y. Toyoshima, and M. de Bono, “Modulation of sensory information processing
by a neuroglobin in Caenorhabditis elegans,” Proceedings of the National Academy
of Sciences, vol. 114, no. 23. National Academy of Sciences, pp. E4658–E4665,
2017.
ista: Oda S, Toyoshima Y, de Bono M. 2017. Modulation of sensory information processing
by a neuroglobin in Caenorhabditis elegans. Proceedings of the National Academy
of Sciences. 114(23), E4658–E4665.
mla: Oda, Shigekazu, et al. “Modulation of Sensory Information Processing by a Neuroglobin
in Caenorhabditis Elegans.” Proceedings of the National Academy of Sciences,
vol. 114, no. 23, National Academy of Sciences, 2017, pp. E4658–65, doi:10.1073/pnas.1614596114.
short: S. Oda, Y. Toyoshima, M. de Bono, Proceedings of the National Academy of
Sciences 114 (2017) E4658–E4665.
date_created: 2019-03-19T13:29:51Z
date_published: 2017-06-06T00:00:00Z
date_updated: 2021-01-12T08:06:11Z
day: '06'
ddc:
- '570'
doi: 10.1073/pnas.1614596114
extern: '1'
external_id:
pmid:
- '28536200'
file:
- access_level: open_access
checksum: 9e42ce47090ecdad7d76f2dbdebb924e
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T13:42:58Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6114'
file_name: 2017_PNAS_Oda.pdf
file_size: 1469622
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 114'
issue: '23'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: E4658-E4665
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
issn:
- 0027-8424
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
status: public
title: Modulation of sensory information processing by a neuroglobin in Caenorhabditis
elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '6115'
abstract:
- lang: eng
text: Animals adjust their behavioral priorities according to momentary needs and
prior experience. We show that Caenorhabditis elegans changes how it processes
sensory information according to the oxygen environment it experienced recently.
C. elegans acclimated to 7% O2 are aroused by CO2 and repelled by pheromones that
attract animals acclimated to 21% O2. This behavioral plasticity arises from prolonged
activity differences in a circuit that continuously signals O2 levels. A sustained
change in the activity of O2-sensing neurons reprograms the properties of their
postsynaptic partners, the RMG hub interneurons. RMG is gap-junctionally coupled
to the ASK and ADL pheromone sensors that respectively drive pheromone attraction
and repulsion. Prior O2 experience has opposite effects on the pheromone responsiveness
of these neurons. These circuit changes provide a physiological correlate of altered
pheromone valence. Our results suggest C. elegans stores a memory of recent O2
experience in the RMG circuit and illustrate how a circuit is flexibly sculpted
to guide behavioral decisions in a context-dependent manner.
author:
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- 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: Fenk LA, de Bono M. Memory of recent oxygen experience switches pheromone valence
inCaenorhabditis elegans. Proceedings of the National Academy of Sciences.
2017;114(16):4195-4200. doi:10.1073/pnas.1618934114
apa: Fenk, L. A., & de Bono, M. (2017). Memory of recent oxygen experience switches
pheromone valence inCaenorhabditis elegans. Proceedings of the National Academy
of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1618934114
chicago: Fenk, Lorenz A., and Mario de Bono. “Memory of Recent Oxygen Experience
Switches Pheromone Valence InCaenorhabditis Elegans.” Proceedings of the National
Academy of Sciences. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1618934114.
ieee: L. A. Fenk and M. de Bono, “Memory of recent oxygen experience switches pheromone
valence inCaenorhabditis elegans,” Proceedings of the National Academy of Sciences,
vol. 114, no. 16. National Academy of Sciences, pp. 4195–4200, 2017.
ista: Fenk LA, de Bono M. 2017. Memory of recent oxygen experience switches pheromone
valence inCaenorhabditis elegans. Proceedings of the National Academy of Sciences.
114(16), 4195–4200.
mla: Fenk, Lorenz A., and Mario de Bono. “Memory of Recent Oxygen Experience Switches
Pheromone Valence InCaenorhabditis Elegans.” Proceedings of the National Academy
of Sciences, vol. 114, no. 16, National Academy of Sciences, 2017, pp. 4195–200,
doi:10.1073/pnas.1618934114.
short: L.A. Fenk, M. de Bono, Proceedings of the National Academy of Sciences 114
(2017) 4195–4200.
date_created: 2019-03-19T13:46:36Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2021-01-12T08:06:11Z
day: '18'
ddc:
- '570'
doi: 10.1073/pnas.1618934114
extern: '1'
external_id:
pmid:
- '28373553'
file:
- access_level: open_access
checksum: 1801bc8319b752fa17598004ec375279
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T14:00:42Z
date_updated: 2020-07-14T12:47:20Z
file_id: '6116'
file_name: 2017_PNAS_Fenk.pdf
file_size: 1217696
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 114'
issue: '16'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 4195-4200
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
issn:
- 0027-8424
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
status: public
title: Memory of recent oxygen experience switches pheromone valence inCaenorhabditis
elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '6117'
abstract:
- lang: eng
text: 'Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates
responses to pathogens or tissue damage, and drives autoimmune diseases. Little
is known about its role in the nervous system. Here we show that IL-17 has neuromodulator-like
properties in Caenorhabditis elegans. IL-17 can act directly on neurons to alter
their response properties and contribution to behaviour. Using unbiased genetic
screens, we delineate an IL-17 signalling pathway and show that it acts in the
RMG hub interneurons. Disrupting IL-17 signalling reduces RMG responsiveness to
input from oxygen sensors, and renders sustained escape from 21% oxygen transient
and contingent on additional stimuli. Over-activating IL-17 receptors abnormally
heightens responses to 21% oxygen in RMG neurons and whole animals. IL-17 deficiency
can be bypassed by optogenetic stimulation of RMG. Inducing IL-17 expression in
adults can rescue mutant defects within 6 h. These findings reveal a non-immunological
role of IL-17 modulating circuit function and behaviour.'
author:
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Eisuke
full_name: Itakura, Eisuke
last_name: Itakura
- first_name: Geoffrey M.
full_name: Nelson, Geoffrey M.
last_name: Nelson
- first_name: Ming
full_name: Sheng, Ming
last_name: Sheng
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- first_name: Rebecca A.
full_name: Butcher, Rebecca A.
last_name: Butcher
- first_name: Ramanujan S.
full_name: Hegde, Ramanujan S.
last_name: Hegde
- 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: Chen C, Itakura E, Nelson GM, et al. IL-17 is a neuromodulator of Caenorhabditis
elegans sensory responses. Nature. 2017;542(7639):43-48. doi:10.1038/nature20818
apa: Chen, C., Itakura, E., Nelson, G. M., Sheng, M., Laurent, P., Fenk, L. A.,
… de Bono, M. (2017). IL-17 is a neuromodulator of Caenorhabditis elegans sensory
responses. Nature. Springer Nature. https://doi.org/10.1038/nature20818
chicago: Chen, Changchun, Eisuke Itakura, Geoffrey M. Nelson, Ming Sheng, Patrick
Laurent, Lorenz A. Fenk, Rebecca A. Butcher, Ramanujan S. Hegde, and Mario de
Bono. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans Sensory Responses.”
Nature. Springer Nature, 2017. https://doi.org/10.1038/nature20818.
ieee: C. Chen et al., “IL-17 is a neuromodulator of Caenorhabditis elegans
sensory responses,” Nature, vol. 542, no. 7639. Springer Nature, pp. 43–48,
2017.
ista: Chen C, Itakura E, Nelson GM, Sheng M, Laurent P, Fenk LA, Butcher RA, Hegde
RS, de Bono M. 2017. IL-17 is a neuromodulator of Caenorhabditis elegans sensory
responses. Nature. 542(7639), 43–48.
mla: Chen, Changchun, et al. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans
Sensory Responses.” Nature, vol. 542, no. 7639, Springer Nature, 2017,
pp. 43–48, doi:10.1038/nature20818.
short: C. Chen, E. Itakura, G.M. Nelson, M. Sheng, P. Laurent, L.A. Fenk, R.A. Butcher,
R.S. Hegde, M. de Bono, Nature 542 (2017) 43–48.
date_created: 2019-03-19T14:06:41Z
date_published: 2017-02-02T00:00:00Z
date_updated: 2021-01-12T08:06:12Z
day: '02'
doi: 10.1038/nature20818
extern: '1'
external_id:
pmid:
- ' 28099418'
intvolume: ' 542'
issue: '7639'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/28099418
month: '02'
oa: 1
oa_version: Submitted Version
page: 43-48
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
- 1476-4687
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 542
year: '2017'
...
---
_id: '6118'
abstract:
- lang: eng
text: 'Carbon dioxide (CO2) gradients are ubiquitous and provide animals with information
about their environment, such as the potential presence of prey or predators.
The nematode Caenorhabditis elegans avoids elevated CO2, and previous work identified
three neuron pairs called “BAG,” “AFD,” and “ASE” that respond to CO2 stimuli.
Using in vivo Ca2+ imaging and behavioral analysis, we show that C. elegans can
detect CO2 independently of these sensory pathways. Many of the C. elegans sensory
neurons we examined, including the AWC olfactory neurons, the ASJ and ASK gustatory
neurons, and the ASH and ADL nociceptors, respond to a rise in CO2 with a rise
in Ca2+. In contrast, glial sheath cells harboring the sensory endings of C. elegans’
major chemosensory neurons exhibit strong and sustained decreases in Ca2+ in response
to high CO2. Some of these CO2 responses appear to be cell intrinsic. Worms therefore
may couple detection of CO2 to that of other cues at the earliest stages of sensory
processing. We show that C. elegans persistently suppresses oviposition at high
CO2. Hermaphrodite-specific neurons (HSNs), the executive neurons driving egg-laying,
are tonically inhibited when CO2 is elevated. CO2 modulates the egg-laying system
partly through the AWC olfactory neurons: High CO2 tonically activates AWC by
a cGMP-dependent mechanism, and AWC output inhibits the HSNs. Our work shows that
CO2 is a more complex sensory cue for C. elegans than previously thought, both
in terms of behavior and neural circuitry.'
author:
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- 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: Fenk LA, de Bono M. Environmental CO2 inhibits Caenorhabditis elegans egg-laying
by modulating olfactory neurons and evokes widespread changes in neural activity.
Proceedings of the National Academy of Sciences. 2015;112(27):E3525-E3534.
doi:10.1073/pnas.1423808112
apa: Fenk, L. A., & de Bono, M. (2015). Environmental CO2 inhibits Caenorhabditis
elegans egg-laying by modulating olfactory neurons and evokes widespread changes
in neural activity. Proceedings of the National Academy of Sciences. National
Academy of Sciences. https://doi.org/10.1073/pnas.1423808112
chicago: Fenk, Lorenz A., and Mario de Bono. “Environmental CO2 Inhibits Caenorhabditis
Elegans Egg-Laying by Modulating Olfactory Neurons and Evokes Widespread Changes
in Neural Activity.” Proceedings of the National Academy of Sciences. National
Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1423808112.
ieee: L. A. Fenk and M. de Bono, “Environmental CO2 inhibits Caenorhabditis elegans
egg-laying by modulating olfactory neurons and evokes widespread changes in neural
activity,” Proceedings of the National Academy of Sciences, vol. 112, no.
27. National Academy of Sciences, pp. E3525–E3534, 2015.
ista: Fenk LA, de Bono M. 2015. Environmental CO2 inhibits Caenorhabditis elegans
egg-laying by modulating olfactory neurons and evokes widespread changes in neural
activity. Proceedings of the National Academy of Sciences. 112(27), E3525–E3534.
mla: Fenk, Lorenz A., and Mario de Bono. “Environmental CO2 Inhibits Caenorhabditis
Elegans Egg-Laying by Modulating Olfactory Neurons and Evokes Widespread Changes
in Neural Activity.” Proceedings of the National Academy of Sciences, vol.
112, no. 27, National Academy of Sciences, 2015, pp. E3525–34, doi:10.1073/pnas.1423808112.
short: L.A. Fenk, M. de Bono, Proceedings of the National Academy of Sciences 112
(2015) E3525–E3534.
date_created: 2019-03-19T14:15:50Z
date_published: 2015-07-07T00:00:00Z
date_updated: 2021-01-12T08:06:12Z
day: '07'
ddc:
- '570'
doi: 10.1073/pnas.1423808112
extern: '1'
external_id:
pmid:
- '26100886'
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creator: kschuh
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language:
- iso: eng
month: '07'
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oa_version: Published Version
page: E3525-E3534
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
issn:
- 0027-8424
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
status: public
title: Environmental CO2 inhibits Caenorhabditis elegans egg-laying by modulating
olfactory neurons and evokes widespread changes in neural activity
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2015'
...
---
_id: '6120'
abstract:
- lang: eng
text: Brains organize behavior and physiology to optimize the response to threats
or opportunities. We dissect how 21% O2, an indicator of surface exposure, reprograms
C. elegans' global state, inducing sustained locomotory arousal and altering expression
of neuropeptides, metabolic enzymes, and other non-neural genes. The URX O2-sensing
neurons drive arousal at 21% O2 by tonically activating the RMG interneurons.
Stimulating RMG is sufficient to switch behavioral state. Ablating the ASH, ADL,
or ASK sensory neurons connected to RMG by gap junctions does not disrupt arousal.
However, disrupting cation currents in these neurons curtails RMG neurosecretion
and arousal. RMG signals high O2 by peptidergic secretion. Neuropeptide reporters
reveal neural circuit state, as neurosecretion stimulates neuropeptide expression.
Neural imaging in unrestrained animals shows that URX and RMG encode O2 concentration
rather than behavior, while the activity of downstream interneurons such as AVB
and AIY reflect both O2 levels and the behavior being executed.
article_number: e04241
author:
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
- first_name: Zoltan
full_name: Soltesz, Zoltan
last_name: Soltesz
- first_name: Geoffrey M
full_name: Nelson, Geoffrey M
last_name: Nelson
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Fausto
full_name: Arellano-Carbajal, Fausto
last_name: Arellano-Carbajal
- first_name: Emmanuel
full_name: Levy, Emmanuel
last_name: Levy
- 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: Laurent P, Soltesz Z, Nelson GM, et al. Decoding a neural circuit controlling
global animal state in C. elegans. eLife. 2015;4. doi:10.7554/elife.04241
apa: Laurent, P., Soltesz, Z., Nelson, G. M., Chen, C., Arellano-Carbajal, F., Levy,
E., & de Bono, M. (2015). Decoding a neural circuit controlling global animal
state in C. elegans. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.04241
chicago: Laurent, Patrick, Zoltan Soltesz, Geoffrey M Nelson, Changchun Chen, Fausto
Arellano-Carbajal, Emmanuel Levy, and Mario de Bono. “Decoding a Neural Circuit
Controlling Global Animal State in C. Elegans.” ELife. eLife Sciences Publications,
2015. https://doi.org/10.7554/elife.04241.
ieee: P. Laurent et al., “Decoding a neural circuit controlling global animal
state in C. elegans,” eLife, vol. 4. eLife Sciences Publications, 2015.
ista: Laurent P, Soltesz Z, Nelson GM, Chen C, Arellano-Carbajal F, Levy E, de Bono
M. 2015. Decoding a neural circuit controlling global animal state in C. elegans.
eLife. 4, e04241.
mla: Laurent, Patrick, et al. “Decoding a Neural Circuit Controlling Global Animal
State in C. Elegans.” ELife, vol. 4, e04241, eLife Sciences Publications,
2015, doi:10.7554/elife.04241.
short: P. Laurent, Z. Soltesz, G.M. Nelson, C. Chen, F. Arellano-Carbajal, E. Levy,
M. de Bono, ELife 4 (2015).
date_created: 2019-03-19T14:23:51Z
date_published: 2015-03-11T00:00:00Z
date_updated: 2021-01-12T08:06:13Z
day: '11'
ddc:
- '570'
doi: 10.7554/elife.04241
extern: '1'
external_id:
pmid:
- '25760081'
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creator: kschuh
date_created: 2019-03-19T14:29:43Z
date_updated: 2020-07-14T12:47:20Z
file_id: '6121'
file_name: 2015_elife_Laurent.pdf
file_size: 6723528
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 4'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Decoding a neural circuit controlling global animal state 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)
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type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 4
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...