---
_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. <i>eLife</i>. 2022;11. doi:<a
    href="https://doi.org/10.7554/eLife.68040">10.7554/eLife.68040</a>
  apa: Valperga, G., &#38; de Bono, M. (2022). Impairing one sensory modality enhances
    another by reconfiguring peptidergic signalling in Caenorhabditis elegans. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.68040">https://doi.org/10.7554/eLife.68040</a>
  chicago: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances
    Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” <i>ELife</i>.
    eLife Sciences Publications, 2022. <a href="https://doi.org/10.7554/eLife.68040">https://doi.org/10.7554/eLife.68040</a>.
  ieee: G. Valperga and M. de Bono, “Impairing one sensory modality enhances another
    by reconfiguring peptidergic signalling in Caenorhabditis elegans,” <i>eLife</i>,
    vol. 11. eLife Sciences Publications, 2022.
  ista: Valperga G, de Bono M. 2022. Impairing one sensory modality enhances another
    by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 11,
    e68040.
  mla: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances
    Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” <i>ELife</i>,
    vol. 11, e68040, eLife Sciences Publications, 2022, doi:<a href="https://doi.org/10.7554/eLife.68040">10.7554/eLife.68040</a>.
  short: G. Valperga, M. de Bono, ELife 11 (2022).
date_created: 2022-03-06T23:01:52Z
date_published: 2022-02-24T00:00:00Z
date_updated: 2023-08-02T14:42:55Z
day: '24'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.7554/eLife.68040
external_id:
  isi:
  - '000763432300001'
  pmid:
  - '35201977'
file:
- access_level: open_access
  checksum: cc1b9bf866d0f61f965556e0dd03d3ac
  content_type: application/pdf
  creator: dernst
  date_created: 2022-03-07T07:39:25Z
  date_updated: 2022-03-07T07:39:25Z
  file_id: '10830'
  file_name: 2022_eLife_Valperga.pdf
  file_size: 4095591
  relation: main_file
  success: 1
file_date_updated: 2022-03-07T07:39:25Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E
  grant_number: 209504/A/17/Z
  name: Molecular mechanisms of neural circuit function
publication: eLife
publication_identifier:
  eissn:
  - 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Impairing one sensory modality enhances another by reconfiguring peptidergic
  signalling in Caenorhabditis elegans
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '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. <i>Behavioral Neurogenetics</i>. Vol 181.
    NM. New York: Springer Nature; 2022:277-294. doi:<a href="https://doi.org/10.1007/978-1-0716-2321-3_15">10.1007/978-1-0716-2321-3_15</a>'
  apa: 'Artan, M., &#38; de Bono, M. (2022). Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling. In D. Yamamoto (Ed.), <i>Behavioral Neurogenetics</i>
    (Vol. 181, pp. 277–294). New York: Springer Nature. <a href="https://doi.org/10.1007/978-1-0716-2321-3_15">https://doi.org/10.1007/978-1-0716-2321-3_15</a>'
  chicago: 'Artan, Murat, and Mario de Bono. “Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling.” In <i>Behavioral Neurogenetics</i>, edited
    by Daisuke Yamamoto, 181:277–94. NM. New York: Springer Nature, 2022. <a href="https://doi.org/10.1007/978-1-0716-2321-3_15">https://doi.org/10.1007/978-1-0716-2321-3_15</a>.'
  ieee: 'M. Artan and M. de Bono, “Proteomic Analysis of C. Elegans Neurons Using
    TurboID-Based Proximity Labeling,” in <i>Behavioral Neurogenetics</i>, vol. 181,
    D. Yamamoto, Ed. New York: Springer Nature, 2022, pp. 277–294.'
  ista: 'Artan M, de Bono M. 2022.Proteomic Analysis of C. Elegans Neurons Using TurboID-Based
    Proximity Labeling. In: Behavioral Neurogenetics. Neuromethods, vol. 181, 277–294.'
  mla: Artan, Murat, and Mario de Bono. “Proteomic Analysis of C. Elegans Neurons
    Using TurboID-Based Proximity Labeling.” <i>Behavioral Neurogenetics</i>, edited
    by Daisuke Yamamoto, vol. 181, Springer Nature, 2022, pp. 277–94, doi:<a href="https://doi.org/10.1007/978-1-0716-2321-3_15">10.1007/978-1-0716-2321-3_15</a>.
  short: M. Artan, M. de Bono, in:, D. Yamamoto (Ed.), Behavioral Neurogenetics, Springer
    Nature, New York, 2022, pp. 277–294.
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. <i>PLoS Biology</i>. 2022;20(6).
    doi:<a href="https://doi.org/10.1371/journal.pbio.3001684">10.1371/journal.pbio.3001684</a>
  apa: Zhao, L., Fenk, L. A., Nilsson, L., Amin-Wetzel, N. P., Ramirez, N., de Bono,
    M., &#38; Chen, C. (2022). ROS and cGMP signaling modulate persistent escape from
    hypoxia in Caenorhabditis elegans. <i>PLoS Biology</i>. Public Library of Science.
    <a href="https://doi.org/10.1371/journal.pbio.3001684">https://doi.org/10.1371/journal.pbio.3001684</a>
  chicago: Zhao, Lina, Lorenz A. Fenk, Lars Nilsson, Niko Paresh Amin-Wetzel, Nelson
    Ramirez, Mario de Bono, and Changchun Chen. “ROS and CGMP Signaling Modulate Persistent
    Escape from Hypoxia in Caenorhabditis Elegans.” <i>PLoS Biology</i>. Public Library
    of Science, 2022. <a href="https://doi.org/10.1371/journal.pbio.3001684">https://doi.org/10.1371/journal.pbio.3001684</a>.
  ieee: L. Zhao <i>et al.</i>, “ROS and cGMP signaling modulate persistent escape
    from hypoxia in Caenorhabditis elegans,” <i>PLoS Biology</i>, vol. 20, no. 6.
    Public Library of Science, 2022.
  ista: Zhao L, Fenk LA, Nilsson L, Amin-Wetzel NP, Ramirez N, de Bono M, Chen C.
    2022. ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis
    elegans. PLoS Biology. 20(6), e3001684.
  mla: Zhao, Lina, et al. “ROS and CGMP Signaling Modulate Persistent Escape from
    Hypoxia in Caenorhabditis Elegans.” <i>PLoS Biology</i>, vol. 20, no. 6, e3001684,
    Public Library of Science, 2022, doi:<a href="https://doi.org/10.1371/journal.pbio.3001684">10.1371/journal.pbio.3001684</a>.
  short: L. Zhao, L.A. Fenk, L. Nilsson, N.P. Amin-Wetzel, N. Ramirez, M. de Bono,
    C. Chen, PLoS Biology 20 (2022).
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. <i>Journal of Biological Chemistry</i>. 2022;298(9). doi:<a
    href="https://doi.org/10.1016/j.jbc.2022.102343">10.1016/j.jbc.2022.102343</a>
  apa: Artan, M., Hartl, M., Chen, W., &#38; de Bono, M. (2022). Depletion of endogenously
    biotinylated carboxylases enhances the sensitivity of TurboID-mediated proximity
    labeling in Caenorhabditis elegans. <i>Journal of Biological Chemistry</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.jbc.2022.102343">https://doi.org/10.1016/j.jbc.2022.102343</a>
  chicago: Artan, Murat, Markus Hartl, Weiqiang Chen, and Mario de Bono. “Depletion
    of Endogenously Biotinylated Carboxylases Enhances the Sensitivity of TurboID-Mediated
    Proximity Labeling in Caenorhabditis Elegans.” <i>Journal of Biological Chemistry</i>.
    Elsevier, 2022. <a href="https://doi.org/10.1016/j.jbc.2022.102343">https://doi.org/10.1016/j.jbc.2022.102343</a>.
  ieee: M. Artan, M. Hartl, W. Chen, and M. de Bono, “Depletion of endogenously biotinylated
    carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
    Caenorhabditis elegans,” <i>Journal of Biological Chemistry</i>, vol. 298, no.
    9. Elsevier, 2022.
  ista: Artan M, Hartl M, Chen W, de Bono M. 2022. Depletion of endogenously biotinylated
    carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in
    Caenorhabditis elegans. Journal of Biological Chemistry. 298(9), 102343.
  mla: Artan, Murat, et al. “Depletion of Endogenously Biotinylated Carboxylases Enhances
    the Sensitivity of TurboID-Mediated Proximity Labeling in Caenorhabditis Elegans.”
    <i>Journal of Biological Chemistry</i>, vol. 298, no. 9, 102343, Elsevier, 2022,
    doi:<a href="https://doi.org/10.1016/j.jbc.2022.102343">10.1016/j.jbc.2022.102343</a>.
  short: M. Artan, M. Hartl, W. Chen, M. de Bono, Journal of Biological Chemistry
    298 (2022).
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publication: Journal of Biological Chemistry
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publisher: Elsevier
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title: Depletion of endogenously biotinylated carboxylases enhances the sensitivity
  of TurboID-mediated proximity labeling in Caenorhabditis elegans
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...
