--- _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: '10826' abstract: - lang: eng text: Animals that lose one sensory modality often show augmented responses to other sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly understood. We probe such mechanisms by performing a forward genetic screen for mutants with enhanced O2 perception in Caenorhabditis elegans. Multiple mutants exhibiting increased O2 responsiveness concomitantly show defects in other sensory responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes pheromone-evoked Ca2+ responses in the ADL pheromone-sensing neurons. At the same time, ADL responsiveness to pre-synaptic input from O2-sensing neurons is heightened in qui-1, and other sensory defective mutants, resulting in enhanced neurosecretion although not increased Ca2+ responses. Expressing qui-1 selectively in ADL rescues both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling ADL neurons in qui-1 mutants highlights extensive changes in gene expression, notably of many neuropeptide receptors. We show that elevated ADL expression of the conserved neuropeptide receptor NPR-22 is necessary for enhanced ADL neurosecretion in qui-1 mutants, and is sufficient to confer increased ADL neurosecretion in control animals. Sensory loss can thus confer cross-modal plasticity by changing the peptidergic connectome. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: ScienComp acknowledgement: "We would like to thank Gemma Chandratillake and Merav Cohen for identifying mutants and José David Moñino Sánchez for his help on neurosecretion assays. We are grateful to Kaveh Ashrafi (UCSF), Piali Sengupta (Brandeis), and the Caenorhabditis Genetic Center (funded by National Institutes of Health Infrastructure Program P40 OD010440) for strains and reagents ... and Rebecca Butcher (Univ. Florida) for C9 pheromone. We thank Tim Stevens, Paula Freire-Pritchett, Alastair Crisp, GurpreetGhattaoraya, and Fabian Amman for help with bioinformatic analysis, Ekaterina Lashmanova for help with injections, Iris Hardege for strains, and Isabel Beets (KU Leuven) and members of the de Bono Lab for comments on the manuscript. We thank the CRUK Cambridge Research Institute Genomics Core for next generation sequencing and the Flow Cytometry Facility at LMB for FACS. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facility (BIF), the Life Science Facility (LSF) and Scientific Computing (SciCo-p– Bioinformatics).\r\nThis work was supported by the Medical Research Council UK (Studentship to GV), an\r\nAdvanced ERC grant (269,058 ACMO to MdB), and a Wellcome Investigator Award (209504/Z/17/Z to MdB)." article_number: e68040 article_processing_charge: No article_type: original author: - first_name: Giulio full_name: Valperga, Giulio id: 67F289DE-0D8F-11EA-9BDD-54AE3DDC885E last_name: Valperga - first_name: Mario full_name: De Bono, Mario id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87 last_name: De Bono orcid: 0000-0001-8347-0443 citation: ama: Valperga G, de Bono M. Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 2022;11. doi:10.7554/eLife.68040 apa: Valperga, G., & de Bono, M. (2022). Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.68040 chicago: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.68040. ieee: G. Valperga and M. de Bono, “Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Valperga G, de Bono M. 2022. Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 11, e68040. mla: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” ELife, vol. 11, e68040, eLife Sciences Publications, 2022, doi:10.7554/eLife.68040. short: G. Valperga, M. de Bono, ELife 11 (2022). date_created: 2022-03-06T23:01:52Z date_published: 2022-02-24T00:00:00Z date_updated: 2023-08-02T14:42:55Z day: '24' ddc: - '570' department: - _id: MaDe doi: 10.7554/eLife.68040 external_id: isi: - '000763432300001' pmid: - '35201977' file: - access_level: open_access checksum: cc1b9bf866d0f61f965556e0dd03d3ac content_type: application/pdf creator: dernst date_created: 2022-03-07T07:39:25Z date_updated: 2022-03-07T07:39:25Z file_id: '10830' file_name: 2022_eLife_Valperga.pdf file_size: 4095591 relation: main_file success: 1 file_date_updated: 2022-03-07T07:39:25Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E grant_number: 209504/A/17/Z name: Molecular mechanisms of neural circuit function publication: eLife publication_identifier: eissn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '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: '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: '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: '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: '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: '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: '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: '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: '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: '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: '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 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: '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: '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: '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' file: - access_level: open_access checksum: 3d2da5af8d72467e382a565abc2e003d content_type: application/pdf creator: kschuh date_created: 2019-03-19T14:21:07Z date_updated: 2020-07-14T12:47:20Z file_id: '6119' file_name: 2015_PNAS_Fenk.pdf file_size: 2822681 relation: main_file file_date_updated: 2020-07-14T12:47:20Z has_accepted_license: '1' intvolume: ' 112' issue: '27' language: - iso: eng month: '07' oa: 1 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' file: - access_level: open_access checksum: cf641b7a363aecd0a101755d23dee7e0 content_type: application/pdf 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) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 4 year: '2015' ...