---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '20929'
abstract:
- lang: eng
text: Insulin/insulin-like growth factor signaling inhibits FOXO transcription factors
to control development, homeostasis, and aging. Here, we use proximity labeling
to identify proteins interacting with the C. elegans FOXO DAF-16. We show that
in well-fed, unstressed animals harboring active insulin signaling, DAF-16 forms
a complex with the PAR-1/MARK serine/threonine kinase, a key regulator of cell
polarity. PAR-1 inhibits DAF-16 accumulation and promotes DAF-16 phosphorylation
at S249, at a conserved motif that PAR-1/human MARK2 phosphorylates in vitro.
DAF-2 insulin-like receptor signaling stimulates DAF-16 S249 phosphorylation,
suggesting DAF-2 activates PAR-1. DAF-2 also promotes PAR-1 expression by inhibiting
DAF-16. PAR-1 knockdown, or DAF-16 S249A, prolong lifespan, whereas phosphomimetic
DAF-16 S249D suppresses the longevity of daf-2 mutants. At low insulin signaling,
DAF-16 proximity labeling highlights transcription factors, chromatin regulators,
and DNA repair proteins. One interactor, the zinc finger/homeobox protein ZFH-2/ZFHX3,
forms a complex with DAF-16 and prolongs lifespan. Our work provides entry points
for hypothesis-driven studies of FOXO function and longevity.
acknowledged_ssus:
- _id: Bio
acknowledgement: We thank de Bono lab members for helpful comments on the manuscript,
and the Mass Spec Facility at the Max Perutz Labs, notably WeiQiang Chen and Markus
Hartl, for invaluable discussions and comments on mass spec analyses of worm samples.
All LC-MS/MS analyses were performed on instruments of the Vienna BioCenter Core
Facilities (VBCF). Microscopy was supported by the Scientific Services Units (SSU)
of ISTA through resources provided by the Imaging & Optics Facility (IOF). We are
grateful to Dr. Geraldine Seydoux (Johns Hopkins University) for worm strains and
plasmids, and Dr. Seung-Jae V. Lee (KAIST) for RNAi clones. We are grateful to Ekaterina
Lashmanova for designing the daf-16::TbID::mNG::3xFLAG knock-in construct and for
her outstanding support in the lab. This work was supported by a Wellcome Investigator
Award (209504/A/17/Z) to MdB and an ISTplus Fellowship to MA (Marie Sklodowska-Curie
agreement No 754411).
article_number: '11355'
article_processing_charge: Yes
article_type: original
author:
- first_name: Murat
full_name: Artan, Murat
id: C407B586-6052-11E9-B3AE-7006E6697425
last_name: Artan
orcid: 0000-0001-8945-6992
- first_name: Hanna
full_name: Schön, Hanna
id: C8E17EDC-D7AA-11E9-B7B7-45ECE5697425
last_name: Schön
- first_name: Mario
full_name: De Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: De Bono
orcid: 0000-0001-8347-0443
citation:
ama: Artan M, Schön H, de Bono M. Proximity labeling of DAF-16 FOXO highlights aging
regulatory proteins. Nature Communications. 2025;16. doi:10.1038/s41467-025-66409-0
apa: Artan, M., Schön, H., & de Bono, M. (2025). Proximity labeling of DAF-16
FOXO highlights aging regulatory proteins. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-025-66409-0
chicago: Artan, Murat, Hanna Schön, and Mario de Bono. “Proximity Labeling of DAF-16
FOXO Highlights Aging Regulatory Proteins.” Nature Communications. Springer
Nature, 2025. https://doi.org/10.1038/s41467-025-66409-0.
ieee: M. Artan, H. Schön, and M. de Bono, “Proximity labeling of DAF-16 FOXO highlights
aging regulatory proteins,” Nature Communications, vol. 16. Springer Nature,
2025.
ista: Artan M, Schön H, de Bono M. 2025. Proximity labeling of DAF-16 FOXO highlights
aging regulatory proteins. Nature Communications. 16, 11355.
mla: Artan, Murat, et al. “Proximity Labeling of DAF-16 FOXO Highlights Aging Regulatory
Proteins.” Nature Communications, vol. 16, 11355, Springer Nature, 2025,
doi:10.1038/s41467-025-66409-0.
short: M. Artan, H. Schön, M. de Bono, Nature Communications 16 (2025).
corr_author: '1'
date_created: 2026-01-04T23:01:34Z
date_published: 2025-12-11T00:00:00Z
date_updated: 2026-01-05T11:00:03Z
day: '11'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1038/s41467-025-66409-0
ec_funded: 1
external_id:
pmid:
- '41381452'
file:
- access_level: open_access
checksum: 748e2e003b878b85b6048d51621d6aae
content_type: application/pdf
creator: dernst
date_created: 2026-01-05T10:58:28Z
date_updated: 2026-01-05T10:58:28Z
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file_size: 1642352
relation: main_file
success: 1
file_date_updated: 2026-01-05T10:58:28Z
has_accepted_license: '1'
intvolume: ' 16'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
grant_number: 209504/A/17/Z
name: Molecular mechanisms of neural circuit function
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Proximity labeling of DAF-16 FOXO highlights aging regulatory proteins
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2025'
...
---
OA_place: publisher
_id: '20167'
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: "This work was supported by EMBO (ALTF 302-2019 to Niko Amin-Wetzel),
the FWF\r\n(ESPRIT PR1054E140 to Niko Amin-Wetzel), the European Research Council\r\n(Advanced
Grant 269058 to Mario de Bono) and Wellcome (209504/A/17/Z\r\nInvestigator Award
to Mario de Bono). "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Hanna
full_name: Schön, Hanna
id: C8E17EDC-D7AA-11E9-B7B7-45ECE5697425
last_name: Schön
citation:
ama: Schön H. The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
GPCRs. 2025. doi:10.15479/AT-ISTA-20167
apa: Schön, H. (2025). The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs
encoding GPCRs. Institute of Science and Technology Austria. https://doi.org/10.15479/AT-ISTA-20167
chicago: Schön, Hanna. “The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs
Encoding GPCRs.” Institute of Science and Technology Austria, 2025. https://doi.org/10.15479/AT-ISTA-20167.
ieee: H. Schön, “The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
GPCRs,” Institute of Science and Technology Austria, 2025.
ista: Schön H. 2025. The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding
GPCRs. Institute of Science and Technology Austria.
mla: Schön, Hanna. The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs Encoding
GPCRs. Institute of Science and Technology Austria, 2025, doi:10.15479/AT-ISTA-20167.
short: H. Schön, The ER Complex SUTU-7/MACO-1 Regulates the Fate of MRNAs Encoding
GPCRs, Institute of Science and Technology Austria, 2025.
corr_author: '1'
date_created: 2025-08-13T11:13:13Z
date_published: 2025-08-13T00:00:00Z
date_updated: 2026-04-07T11:50:26Z
day: '13'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: MaDe
doi: 10.15479/AT-ISTA-20167
file:
- access_level: closed
checksum: b40c74404b8d9593802dabf57bfdf10f
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: hschoen
date_created: 2025-09-08T14:33:50Z
date_updated: 2025-09-09T08:57:04Z
file_id: '20311'
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file_size: 78812587
relation: source_file
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checksum: 16abc3ff66396ce2457fe07ffa8bed90
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date_updated: 2025-09-18T14:12:29Z
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embargo_to: open_access
file_id: '20347'
file_name: 2025_Schoen_Hanna_Thesis.pdf
file_size: 9667057
relation: main_file
file_date_updated: 2025-09-18T14:12:29Z
has_accepted_license: '1'
language:
- iso: eng
month: '08'
oa_version: Published Version
page: '171'
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
grant_number: 209504/A/17/Z
name: Molecular mechanisms of neural circuit function
- _id: 23813290-32DE-11EA-91FC-C7463DDC885E
grant_number: ALTF 302-2019
name: Control of gene expression at the endoplasmic reticulum
publication_identifier:
isbn:
- 978-3-99078-061-9
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
status: public
supervisor:
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
title: The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding GPCRs
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2025'
...
---
_id: '11456'
abstract:
- lang: eng
text: The proteomes of specialized structures, and the interactomes of proteins
of interest, provide entry points to elucidate the functions of molecular machines.
Here, we review a proximity-labeling strategy that uses the improved E. coli biotin
ligase TurboID to characterize C. elegans protein complexes. Although the focus
is on C. elegans neurons, the method is applicable regardless of cell type. We
describe detailed extraction procedures that solubilize the bulk of C. elegans
proteins and highlight the importance of tagging endogenous genes, to ensure physiological
expression levels. We review issues associated with non-specific background noise
and the importance of appropriate controls. As proof of principle, we review our
analysis of the interactome of a presynaptic active zone protein, ELKS-1. Our
aim is to provide a detailed protocol for TurboID-based proximity labeling in
C. elegans and to highlight its potential and its limitations to characterize
protein complexes and subcellular compartments in this animal.
acknowledgement: We thank de Bono lab members for the helpful comments on the manuscript.
The biotin-auxotrophic E. coli strain MG1655bioB:kan was a generous gift from J.
Cronan (University of Illinois) and was kindly sent to us by Jessica Feldman and
Ariana Sanchez (Stanford University). dg398 pEntryslot2_mNeongreen::3XFLAG::stop
and dg397 pEntryslot3_mNeongreen::3XFLAG::stop::unc-54 3’UTR entry vector were kindly
sent by Dr. Dominique Glauser (University of Fribourg). This work was supported
by an Advanced ERC Grant (269058 ACMO) and a Wellcome Investigator Award (209504/Z/17/Z)
to MdB and an ISTplus Fellowship to MA (Marie Sklodowska-Curie agreement No 754411).
alternative_title:
- Neuromethods
article_processing_charge: No
author:
- first_name: Murat
full_name: Artan, Murat
id: C407B586-6052-11E9-B3AE-7006E6697425
last_name: Artan
orcid: 0000-0001-8945-6992
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: 'Artan M, de Bono M. Proteomic Analysis of C. Elegans Neurons Using TurboID-Based
Proximity Labeling. In: Yamamoto D, ed. 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.
corr_author: '1'
date_created: 2022-06-20T08:10:34Z
date_published: 2022-06-04T00:00:00Z
date_updated: 2025-04-14T07:43:58Z
day: '04'
department:
- _id: MaDe
doi: 10.1007/978-1-0716-2321-3_15
ec_funded: 1
editor:
- first_name: Daisuke
full_name: Yamamoto, Daisuke
last_name: Yamamoto
intvolume: ' 181'
language:
- iso: eng
month: '06'
oa_version: None
page: 277-294
place: New York
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
grant_number: 209504/A/17/Z
name: Molecular mechanisms of neural circuit function
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: Behavioral Neurogenetics
publication_identifier:
eisbn:
- '9781071623213'
eissn:
- 1940-6045
isbn:
- '9781071623206'
issn:
- 0893-2336
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
series_title: NM
status: public
title: Proteomic Analysis of C. Elegans Neurons Using TurboID-Based Proximity Labeling
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 181
year: '2022'
...
---
_id: '11637'
abstract:
- lang: eng
text: The ability to detect and respond to acute oxygen (O2) shortages is indispensable
to aerobic life. The molecular mechanisms and circuits underlying this capacity
are poorly understood. Here, we characterize the behavioral responses of feeding
Caenorhabditis elegans to approximately 1% O2. Acute hypoxia triggers a bout of
turning maneuvers followed by a persistent switch to rapid forward movement as
animals seek to avoid and escape hypoxia. While the behavioral responses to 1%
O2 closely resemble those evoked by 21% O2, they have distinct molecular and circuit
underpinnings. Disrupting phosphodiesterases (PDEs), specific G proteins, or BBSome
function inhibits escape from 1% O2 due to increased cGMP signaling. A primary
source of cGMP is GCY-28, the ortholog of the atrial natriuretic peptide (ANP)
receptor. cGMP activates the protein kinase G EGL-4 and enhances neuroendocrine
secretion to inhibit acute responses to 1% O2. Triggering a rise in cGMP optogenetically
in multiple neurons, including AIA interneurons, rapidly and reversibly inhibits
escape from 1% O2. Ca2+ imaging reveals that a 7% to 1% O2 stimulus evokes a Ca2+
decrease in several neurons. Defects in mitochondrial complex I (MCI) and mitochondrial
complex I (MCIII), which lead to persistently high reactive oxygen species (ROS),
abrogate acute hypoxia responses. In particular, repressing the expression of
isp-1, which encodes the iron sulfur protein of MCIII, inhibits escape from 1%
O2 without affecting responses to 21% O2. Both genetic and pharmacological up-regulation
of mitochondrial ROS increase cGMP levels, which contribute to the reduced hypoxia
responses. Our results implicate ROS and precise regulation of intracellular cGMP
in the modulation of acute responses to hypoxia by C. elegans.
acknowledgement: ' This work was funded by H2020 European Research Council (ERC Advanced
grant, 269058 ACMO, https://erc.europa.eu/funding/advanced-grants) and Wellcome
Trust UK (Wellcome Investigator Award, 209504/Z/17/Z, https://wellcome.org/grant-funding/people-and-projects/grants-awarded/molecular-mechanisms-neural-circuit-function-0)
to M.d.B, and by H2020 European Research Council (ERC starting grant, 802653 OXYGEN
SENSING, https://erc.europa.eu/funding/starting-grants) and Vetenskapsrådet (VR
starting grant, 2018-02216, https://www.vr.se/english.html) to C.C. The funders
had no role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.'
article_number: e3001684
article_processing_charge: No
article_type: original
author:
- first_name: Lina
full_name: Zhao, Lina
last_name: Zhao
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- first_name: Lars
full_name: Nilsson, Lars
last_name: Nilsson
- first_name: Niko Paresh
full_name: Amin-Wetzel, Niko Paresh
id: E95D3014-9D8C-11E9-9C80-D2F8E5697425
last_name: Amin-Wetzel
- first_name: Nelson
full_name: Ramirez, Nelson
id: 39831956-E4FE-11E9-85DE-0DC7E5697425
last_name: Ramirez
- first_name: Mario
full_name: De Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: De Bono
orcid: 0000-0001-8347-0443
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
citation:
ama: Zhao L, Fenk LA, Nilsson L, et al. ROS and cGMP signaling modulate persistent
escape from hypoxia in Caenorhabditis elegans. 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).
corr_author: '1'
date_created: 2022-07-24T22:01:42Z
date_published: 2022-06-21T00:00:00Z
date_updated: 2025-04-15T07:32:21Z
day: '21'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1371/journal.pbio.3001684
external_id:
isi:
- '000828679600001'
pmid:
- '35727855'
file:
- access_level: open_access
checksum: df4902f854ad76769d3203bfdc69f16c
content_type: application/pdf
creator: dernst
date_created: 2022-07-25T07:38:49Z
date_updated: 2022-07-25T07:38:49Z
file_id: '11643'
file_name: 2022_PLoSBiology_Zhao.pdf
file_size: 3721585
relation: main_file
success: 1
file_date_updated: 2022-07-25T07:38:49Z
has_accepted_license: '1'
intvolume: ' 20'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
grant_number: 209504/A/17/Z
name: Molecular mechanisms of neural circuit function
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis
elegans
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_id: '12082'
abstract:
- lang: eng
text: Proximity-dependent protein labeling provides a powerful in vivo strategy
to characterize the interactomes of specific proteins. We previously optimized
a proximity labeling protocol for Caenorhabditis elegans using the highly active
biotin ligase TurboID. A significant constraint on the sensitivity of TurboID
is the presence of abundant endogenously biotinylated proteins that take up bandwidth
in the mass spectrometer, notably carboxylases that use biotin as a cofactor.
In C. elegans, these comprise POD-2/acetyl-CoA carboxylase alpha, PCCA-1/propionyl-CoA
carboxylase alpha, PYC-1/pyruvate carboxylase, and MCCC-1/methylcrotonyl-CoA carboxylase
alpha. Here, we developed ways to remove these carboxylases prior to streptavidin
purification and mass spectrometry by engineering their corresponding genes to
add a C-terminal His10 tag. This allows us to deplete them from C. elegans lysates
using immobilized metal affinity chromatography. To demonstrate the method's efficacy,
we use it to expand the interactome map of the presynaptic active zone protein
ELKS-1. We identify many known active zone proteins, including UNC-10/RIM, SYD-2/liprin-alpha,
SAD-1/BRSK1, CLA-1/CLArinet, C16E9.2/Sentryn, as well as previously uncharacterized
potentially synaptic proteins such as the ortholog of human angiomotin, F59C12.3
and the uncharacterized protein R148.3. Our approach provides a quick and inexpensive
solution to a common contaminant problem in biotin-dependent proximity labeling.
The approach may be applicable to other model organisms and will enable deeper
and more complete analysis of interactors for proteins of interest.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank de Bono laboratory members for helpful comments on the
article and the Mass Spec Facilities at IST Austria and Max Perutz Labs for invaluable
discussions and comments on how to optimize mass spec analyses of worm samples.
We are grateful to Ekaterina Lashmanova for designing the degron knock-in constructs
and preparing the injection mixes for CRISPR/Cas9-mediated genome editing. All LC–MS/MS
analyses were performed on instruments of the Vienna BioCenter Core Facilities instrument
pool.\r\nThis work was supported by a Wellcome Investigator Award (grant no.: 209504/Z/17/Z
) to M.d.B. and an ISTplus Fellowship to M.A. (Marie Sklodowska-Curie agreement
no.: 754411)."
article_number: '102343'
article_processing_charge: No
article_type: original
author:
- first_name: Murat
full_name: Artan, Murat
id: C407B586-6052-11E9-B3AE-7006E6697425
last_name: Artan
orcid: 0000-0001-8945-6992
- first_name: Markus
full_name: Hartl, Markus
last_name: Hartl
- first_name: Weiqiang
full_name: Chen, Weiqiang
last_name: Chen
- first_name: Mario
full_name: De Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: De Bono
orcid: 0000-0001-8347-0443
citation:
ama: Artan M, Hartl M, Chen W, de Bono M. Depletion of endogenously biotinylated
carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
Caenorhabditis elegans. 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).
corr_author: '1'
date_created: 2022-09-11T22:01:55Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2025-04-14T07:44:00Z
day: '01'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1016/j.jbc.2022.102343
ec_funded: 1
external_id:
isi:
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pmid:
- '35933017'
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file_size: 2101656
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- 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: '10826'
abstract:
- lang: eng
text: Animals that lose one sensory modality often show augmented responses to other
sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly
understood. We probe such mechanisms by performing a forward genetic screen for
mutants with enhanced O2 perception in Caenorhabditis elegans. Multiple mutants
exhibiting increased O2 responsiveness concomitantly show defects in other sensory
responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes
pheromone-evoked Ca2+ responses in the ADL pheromone-sensing neurons. At the same
time, ADL responsiveness to pre-synaptic input from O2-sensing neurons is heightened
in qui-1, and other sensory defective mutants, resulting in enhanced neurosecretion
although not increased Ca2+ responses. Expressing qui-1 selectively in ADL rescues
both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling
ADL neurons in qui-1 mutants highlights extensive changes in gene expression,
notably of many neuropeptide receptors. We show that elevated ADL expression of
the conserved neuropeptide receptor NPR-22 is necessary for enhanced ADL neurosecretion
in qui-1 mutants, and is sufficient to confer increased ADL neurosecretion in
control animals. Sensory loss can thus confer cross-modal plasticity by changing
the peptidergic connectome.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: ScienComp
acknowledgement: "We would like to thank Gemma Chandratillake and Merav Cohen for
identifying mutants and José David Moñino Sánchez for his help on neurosecretion
assays. We are grateful to Kaveh Ashrafi (UCSF), Piali Sengupta (Brandeis), and
the Caenorhabditis Genetic Center (funded by National Institutes of Health Infrastructure
Program P40 OD010440) for strains and reagents ... and Rebecca Butcher (Univ. Florida)
for C9 pheromone. We thank Tim Stevens, Paula Freire-Pritchett, Alastair Crisp,
GurpreetGhattaoraya, and Fabian Amman for help with bioinformatic analysis, Ekaterina
Lashmanova for help with injections, Iris Hardege for strains, and Isabel Beets
(KU Leuven) and members of the de Bono Lab for comments on the manuscript. We thank
the CRUK Cambridge Research Institute Genomics Core for next generation sequencing
and the Flow Cytometry Facility at LMB for FACS. This research was supported by
the Scientific Service Units (SSU) of IST Austria through resources provided by
the Bioimaging Facility (BIF), the Life Science Facility (LSF) and Scientific Computing
(SciCo-p– Bioinformatics).\r\nThis work was supported by the Medical Research Council
UK (Studentship to GV), an\r\nAdvanced ERC grant (269,058 ACMO to MdB), and a Wellcome
Investigator Award (209504/Z/17/Z to MdB)."
article_number: e68040
article_processing_charge: No
article_type: original
author:
- first_name: Giulio
full_name: Valperga, Giulio
id: 67F289DE-0D8F-11EA-9BDD-54AE3DDC885E
last_name: Valperga
orcid: 0000-0001-6726-3890
- first_name: Mario
full_name: De Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: De Bono
orcid: 0000-0001-8347-0443
citation:
ama: Valperga G, de Bono M. Impairing one sensory modality enhances another by reconfiguring
peptidergic signalling in Caenorhabditis elegans. 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).
corr_author: '1'
date_created: 2022-03-06T23:01:52Z
date_published: 2022-02-24T00:00:00Z
date_updated: 2026-04-02T12:45:39Z
day: '24'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.7554/eLife.68040
external_id:
isi:
- '000763432300001'
pmid:
- '35201977'
file:
- access_level: open_access
checksum: cc1b9bf866d0f61f965556e0dd03d3ac
content_type: application/pdf
creator: dernst
date_created: 2022-03-07T07:39:25Z
date_updated: 2022-03-07T07:39:25Z
file_id: '10830'
file_name: 2022_eLife_Valperga.pdf
file_size: 4095591
relation: main_file
success: 1
file_date_updated: 2022-03-07T07:39:25Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
grant_number: 209504/A/17/Z
name: Molecular mechanisms of neural circuit function
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Impairing one sensory modality enhances another by reconfiguring peptidergic
signalling in Caenorhabditis elegans
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 11
year: '2022'
...