--- _id: '15016' abstract: - lang: eng text: 'The development, evolution, and function of the vertebrate central nervous system (CNS) can be best studied using diverse model organisms. Amphibians, with their unique phylogenetic position at the transition between aquatic and terrestrial lifestyles, are valuable for understanding the origin and evolution of the tetrapod brain and spinal cord. Their metamorphic developmental transitions and unique regenerative abilities also facilitate the discovery of mechanisms for neural circuit remodeling and replacement. The genetic toolkit for amphibians, however, remains limited, with only a few species having sequenced genomes and a small number of transgenic lines available. In mammals, recombinant adeno-associated viral vectors (AAVs) have become a powerful alternative to genome modification for visualizing and perturbing the nervous system. AAVs are DNA viruses that enable neuronal transduction in both developing and adult animals with low toxicity and spatial, temporal, and cell-type specificity. However, AAVs have never been shown to transduce amphibian cells efficiently. To bridge this gap, we established a simple, scalable, and robust strategy to screen AAV serotypes in three distantly-related amphibian species: the frogs Xenopus laevis and Pelophylax bedriagae, and the salamander Pleurodeles waltl, in both developing larval tadpoles and post-metamorphic animals. For each species, we successfully identified at least two AAV serotypes capable of infecting the CNS; however, no pan-amphibian serotype was identified, indicating rapid evolution of AAV tropism. In addition, we developed an AAV-based strategy that targets isochronic cohorts of developing neurons – a critical tool for parsing neural circuit assembly. Finally, to enable visualization and manipulation of neural circuits, we identified AAV variants for retrograde tracing of neuronal projections in adult animals. Our findings expand the toolkit for amphibians to include AAVs, establish a generalizable workflow for AAV screening in non-canonical research organisms, generate testable hypotheses for the evolution of AAV tropism, and lay the foundation for modern cross-species comparisons of vertebrate CNS development, function, and evolution. ' acknowledgement: "We would like to extend our thanks to members of the Sweeney, Tosches, Shein-Idelson,\r\nYamaguchi, Kelley, and Cline Labs for their contributions to this project, discussion and support.\r\nWe additionally thank the Beckman Institute Clover Center and Viviana Gradinaru (Caltech),\r\nKimberly Ritola (UNC NeuroTools), Flavia Gama Gomez Leite (ISTA Viral Core), and Hüseyin\r\nCihan Önal (Shigemoto Group, ISTA) for their consultation and assistance regarding AAVs, as\r\nwell as Andras Simon and Alberto Joven for feedback and discussions on AAVs in Pleurodeles.\r\nTo do these experiments, we have also benefited from the tremendous support of our animal care and imaging facilities at our respective institutions, as well as the amphibian stock centers\r\n(National Xenopus Resource Center, European Xenopus Resource Center, Xenopus Express)\r\nand our funding sources: U.S. National Science Foundation (NSF) Grant Number IOS 2110086\r\n(D.B.K., L.B.S., M.A.T., A.Y., and H.T.C.); United States-Israel Binational Science Foundation\r\n(BSF) Grant Number 2020702 (M.S.-I.); NSF Award Number 1645105 (G.J.G., M.E.H.); FTI\r\nStrategy Lower Austria Dissertation Grant Number FTI21-D-046 (D.V.); Horizon Europe ERC\r\nStarting Grant Number 101041551 (L.B.S.); NIH grant number R35GM146973 (M.A.T.); Rita Allen\r\nFoundation award number GA_032522_FE (M.A.T.); European Molecular Biology Organization\r\nLong-Term Fellowship ALTF 874-2021 (A.D.); National Science Foundation Graduate Research\r\nFellowship DGE 2036197 (E.C.J.B.); NIH grant number P40OD010997 (M.E.H)." article_processing_charge: No author: - first_name: Eliza C.B. full_name: Jaeger, Eliza C.B. last_name: Jaeger - first_name: David full_name: Vijatovic, David id: cf391e77-ec3c-11ea-a124-d69323410b58 last_name: Vijatovic - first_name: Astrid full_name: Deryckere, Astrid last_name: Deryckere - first_name: Nikol full_name: Zorin, Nikol last_name: Zorin - first_name: Akemi L. full_name: Nguyen, Akemi L. last_name: Nguyen - first_name: Georgiy full_name: Ivanian, Georgiy id: eaf2b366-cfd1-11ee-bbdf-c8790f800a05 last_name: Ivanian - first_name: Jamie full_name: Woych, Jamie last_name: Woych - first_name: Rebecca C full_name: Arnold, Rebecca C id: d6cce458-14c9-11ed-a755-c1c8fc6fde6f last_name: Arnold - first_name: Alonso full_name: Ortega Gurrola, Alonso last_name: Ortega Gurrola - first_name: Arik full_name: Shvartsman, Arik last_name: Shvartsman - first_name: Francesca full_name: Barbieri, Francesca id: a9492887-8972-11ed-ae7b-bfae10998254 last_name: Barbieri - first_name: Florina-Alexandra full_name: Toma, Florina-Alexandra id: 85dd99f2-15b2-11ec-abd3-d1ae4d57f3b5 last_name: Toma - first_name: Gary J. full_name: Gorbsky, Gary J. last_name: Gorbsky - first_name: Marko E. full_name: Horb, Marko E. last_name: Horb - first_name: Hollis T. full_name: Cline, Hollis T. last_name: Cline - first_name: Timothy F. full_name: Shay, Timothy F. last_name: Shay - first_name: Darcy B. full_name: Kelley, Darcy B. last_name: Kelley - first_name: Ayako full_name: Yamaguchi, Ayako last_name: Yamaguchi - first_name: Mark full_name: Shein-Idelson, Mark last_name: Shein-Idelson - first_name: Maria Antonietta full_name: Tosches, Maria Antonietta last_name: Tosches - first_name: Lora Beatrice Jaeger full_name: Sweeney, Lora Beatrice Jaeger id: 56BE8254-C4F0-11E9-8E45-0B23E6697425 last_name: Sweeney orcid: 0000-0001-9242-5601 citation: ama: Jaeger ECB, Vijatovic D, Deryckere A, et al. Adeno-associated viral tools to trace neural development and connectivity across amphibians. bioRxiv. doi:10.1101/2024.02.15.580289 apa: Jaeger, E. C. B., Vijatovic, D., Deryckere, A., Zorin, N., Nguyen, A. L., Ivanian, G., … Sweeney, L. B. (n.d.). Adeno-associated viral tools to trace neural development and connectivity across amphibians. bioRxiv. https://doi.org/10.1101/2024.02.15.580289 chicago: Jaeger, Eliza C.B., David Vijatovic, Astrid Deryckere, Nikol Zorin, Akemi L. Nguyen, Georgiy Ivanian, Jamie Woych, et al. “Adeno-Associated Viral Tools to Trace Neural Development and Connectivity across Amphibians.” BioRxiv, n.d. https://doi.org/10.1101/2024.02.15.580289. ieee: E. C. B. Jaeger et al., “Adeno-associated viral tools to trace neural development and connectivity across amphibians,” bioRxiv. . ista: Jaeger ECB, Vijatovic D, Deryckere A, Zorin N, Nguyen AL, Ivanian G, Woych J, Arnold RC, Ortega Gurrola A, Shvartsman A, Barbieri F, Toma F-A, Gorbsky GJ, Horb ME, Cline HT, Shay TF, Kelley DB, Yamaguchi A, Shein-Idelson M, Tosches MA, Sweeney LB. Adeno-associated viral tools to trace neural development and connectivity across amphibians. bioRxiv, 10.1101/2024.02.15.580289. mla: Jaeger, Eliza C. B., et al. “Adeno-Associated Viral Tools to Trace Neural Development and Connectivity across Amphibians.” BioRxiv, doi:10.1101/2024.02.15.580289. short: E.C.B. Jaeger, D. Vijatovic, A. Deryckere, N. Zorin, A.L. Nguyen, G. Ivanian, J. Woych, R.C. Arnold, A. Ortega Gurrola, A. Shvartsman, F. Barbieri, F.-A. Toma, G.J. Gorbsky, M.E. Horb, H.T. Cline, T.F. Shay, D.B. Kelley, A. Yamaguchi, M. Shein-Idelson, M.A. Tosches, L.B. Sweeney, BioRxiv (n.d.). date_created: 2024-02-20T09:20:32Z date_published: 2024-02-16T00:00:00Z date_updated: 2024-02-20T09:34:25Z day: '16' department: - _id: LoSw - _id: MaDe - _id: GaNo doi: 10.1101/2024.02.15.580289 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2024.02.15.580289 month: '02' oa: 1 oa_version: Preprint project: - _id: bd73af52-d553-11ed-ba76-912049f0ac7a grant_number: FTI21-D-046 name: Entwicklung und Funktion der V1 Interneuronen vom Schwimmen zum Laufen während der Metamorphose von Xenopus - _id: ebb66355-77a9-11ec-83b8-b8ac210a4dae grant_number: '101041551' name: Development and Evolution of Tetrapod Motor Circuits publication: bioRxiv publication_status: submitted status: public title: Adeno-associated viral tools to trace neural development and connectivity across amphibians type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2024' ... --- _id: '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: '12275' abstract: - lang: eng text: N-glycans are molecularly diverse sugars borne by over 70% of proteins transiting the secretory pathway and have been implicated in protein folding, stability, and localization. Mutations in genes important for N-glycosylation result in congenital disorders of glycosylation that are often associated with intellectual disability. Here, we show that structurally distinct N-glycans regulate an extracellular protein complex involved in the patterning of somatosensory dendrites in Caenorhabditis elegans. Specifically, aman-2/Golgi alpha-mannosidase II, a conserved key enzyme in the biosynthesis of specific N-glycans, regulates the activity of the Menorin adhesion complex without obviously affecting the protein stability and localization of its components. AMAN-2 functions cell-autonomously to allow for decoration of the neuronal transmembrane receptor DMA-1/LRR-TM with the correct set of high-mannose/hybrid/paucimannose N-glycans. Moreover, distinct types of N-glycans on specific N-glycosylation sites regulate DMA-1/LRR-TM receptor function, which, together with three other extracellular proteins, forms the Menorin adhesion complex. In summary, specific N-glycan structures regulate dendrite patterning by coordinating the activity of an extracellular adhesion complex, suggesting that the molecular diversity of N-glycans can contribute to developmental specificity in the nervous system. acknowledgement: 'We thank Scott Garforth, Sarah Garrett, Peri Kurshan, Yehuda Salzberg, PamelaStanley, Robert Townley, and members of the B€ulow laboratory for commentson the manuscript or helpful discussions during the course of this work. Wethank David Miller, Shohei Mitani, Kang Shen, and Iain Wilson for reagents,and Yuji Kohara for theyk11g705cDNA clone. We are grateful to MeeraTrivedi for sharing thedzIs117strain prior to publication. Some strains wereprovided by the Caenorhabditis Genome Center (funded by the NIH Office ofResearch Infrastructure Programs P40OD010440). This work was supportedby grants from the National Institute of Health (NIH): R01NS096672andR21NS111145to HEB; F31NS100370to MR; T32GM007288and F31HD066967to CADB; P30HD071593to Albert Einstein College of Medicine. We acknowl-edge support to MR by the Department of Neuroscience. NJRS was the recipi-ent of a Colciencias-Fulbright Fellowship and HEB of an Irma T. Hirschl/Monique Weill-Caulier research fellowship' article_number: e54163 article_processing_charge: No article_type: original author: - first_name: Maisha full_name: Rahman, Maisha last_name: Rahman - first_name: Nelson full_name: Ramirez, Nelson id: 39831956-E4FE-11E9-85DE-0DC7E5697425 last_name: Ramirez - first_name: Carlos A full_name: Diaz‐Balzac, Carlos A last_name: Diaz‐Balzac - first_name: Hannes E full_name: Bülow, Hannes E last_name: Bülow citation: ama: Rahman M, Ramirez N, Diaz‐Balzac CA, Bülow HE. Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning. EMBO Reports. 2022;23(7). doi:10.15252/embr.202154163 apa: Rahman, M., Ramirez, N., Diaz‐Balzac, C. A., & Bülow, H. E. (2022). Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning. EMBO Reports. Embo Press. https://doi.org/10.15252/embr.202154163 chicago: Rahman, Maisha, Nelson Ramirez, Carlos A Diaz‐Balzac, and Hannes E Bülow. “Specific N-Glycans Regulate an Extracellular Adhesion Complex during Somatosensory Dendrite Patterning.” EMBO Reports. Embo Press, 2022. https://doi.org/10.15252/embr.202154163. ieee: M. Rahman, N. Ramirez, C. A. Diaz‐Balzac, and H. E. Bülow, “Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning,” EMBO Reports, vol. 23, no. 7. Embo Press, 2022. ista: Rahman M, Ramirez N, Diaz‐Balzac CA, Bülow HE. 2022. Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning. EMBO Reports. 23(7), e54163. mla: Rahman, Maisha, et al. “Specific N-Glycans Regulate an Extracellular Adhesion Complex during Somatosensory Dendrite Patterning.” EMBO Reports, vol. 23, no. 7, e54163, Embo Press, 2022, doi:10.15252/embr.202154163. short: M. Rahman, N. Ramirez, C.A. Diaz‐Balzac, H.E. Bülow, EMBO Reports 23 (2022). date_created: 2023-01-16T10:01:44Z date_published: 2022-07-05T00:00:00Z date_updated: 2023-10-03T11:25:54Z day: '05' department: - _id: MaDe doi: 10.15252/embr.202154163 external_id: isi: - '000797302700001' pmid: - '35586945' has_accepted_license: '1' intvolume: ' 23' isi: 1 issue: '7' keyword: - Genetics - Molecular Biology - Biochemistry language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.15252/embr.202154163 month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: EMBO Reports publication_identifier: eissn: - 1469-3178 issn: - 1469-221X publication_status: published publisher: Embo Press quality_controlled: '1' scopus_import: '1' status: public title: Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 23 year: '2022' ... --- _id: '10846' abstract: - lang: eng text: The Golgi apparatus regulates the process of modification and subcellular localization of macromolecules, including proteins and lipids. Aberrant protein sorting caused by defects in the Golgi leads to various diseases in mammals. However, the role of the Golgi apparatus in organismal longevity remained largely unknown. By employing a quantitative proteomic approach, we demonstrated that MON-2, an evolutionarily conserved Arf-GEF protein implicated in Golgi-to-endosome trafficking, promotes longevity via upregulating macroautophagy/autophagy in C. elegans. Our data using cultured mammalian cells indicate that MON2 translocates from the Golgi to the endosome under starvation conditions, subsequently increasing autophagic flux by binding LGG-1/GABARAPL2. Thus, Golgi-to-endosome trafficking appears to be an evolutionarily conserved process for the upregulation of autophagy, which contributes to organismal longevity. acknowledgement: This work is funded by National Research Foundation of Korea (NRF) grants NRF-2019R1A3B2067745 from the Korean Government (Ministry of Science and Information and Communications Technology (S-J.V.L.). NRF-2017R1A5A1015366 (S.Y.P, S-J.V.L). Korea Institute of Science and Technology (KIST) intramural grant (C.L). article_processing_charge: No article_type: original author: - first_name: Murat full_name: Artan, Murat id: C407B586-6052-11E9-B3AE-7006E6697425 last_name: Artan orcid: 0000-0001-8945-6992 - first_name: Jooyeon full_name: Sohn, Jooyeon last_name: Sohn - first_name: Cheolju full_name: Lee, Cheolju last_name: Lee - first_name: Seung Yeol full_name: Park, Seung Yeol last_name: Park - first_name: Seung Jae V. full_name: Lee, Seung Jae V. last_name: Lee citation: ama: Artan M, Sohn J, Lee C, Park SY, Lee SJV. MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications. Autophagy. 2022;18(5):1208-1210. doi:10.1080/15548627.2022.2039523 apa: Artan, M., Sohn, J., Lee, C., Park, S. Y., & Lee, S. J. V. (2022). MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications. Autophagy. Taylor & Francis. https://doi.org/10.1080/15548627.2022.2039523 chicago: Artan, Murat, Jooyeon Sohn, Cheolju Lee, Seung Yeol Park, and Seung Jae V. Lee. “MON-2, a Golgi Protein, Promotes Longevity by Upregulating Autophagy through Mediating Inter-Organelle Communications.” Autophagy. Taylor & Francis, 2022. https://doi.org/10.1080/15548627.2022.2039523. ieee: M. Artan, J. Sohn, C. Lee, S. Y. Park, and S. J. V. Lee, “MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications,” Autophagy, vol. 18, no. 5. Taylor & Francis, pp. 1208–1210, 2022. ista: Artan M, Sohn J, Lee C, Park SY, Lee SJV. 2022. MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications. Autophagy. 18(5), 1208–1210. mla: Artan, Murat, et al. “MON-2, a Golgi Protein, Promotes Longevity by Upregulating Autophagy through Mediating Inter-Organelle Communications.” Autophagy, vol. 18, no. 5, Taylor & Francis, 2022, pp. 1208–10, doi:10.1080/15548627.2022.2039523. short: M. Artan, J. Sohn, C. Lee, S.Y. Park, S.J.V. Lee, Autophagy 18 (2022) 1208–1210. date_created: 2022-03-13T23:01:47Z date_published: 2022-02-19T00:00:00Z date_updated: 2023-10-03T10:54:54Z day: '19' department: - _id: MaDe doi: 10.1080/15548627.2022.2039523 external_id: isi: - '000758859600001' pmid: - '35188063' intvolume: ' 18' isi: 1 issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1080/15548627.2022.2039523 month: '02' oa: 1 oa_version: Published Version page: 1208-1210 pmid: 1 publication: Autophagy publication_identifier: eissn: - 1554-8635 issn: - 1554-8627 publication_status: published publisher: Taylor & Francis quality_controlled: '1' scopus_import: '1' status: public title: MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 18 year: '2022' ... --- _id: '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: '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: '15057' abstract: - lang: eng text: Vaccinia virus–related kinase (VRK) is an evolutionarily conserved nuclear protein kinase. VRK-1, the single Caenorhabditis elegans VRK ortholog, functions in cell division and germline proliferation. However, the role of VRK-1 in postmitotic cells and adult life span remains unknown. Here, we show that VRK-1 increases organismal longevity by activating the cellular energy sensor, AMP-activated protein kinase (AMPK), via direct phosphorylation. We found that overexpression of vrk-1 in the soma of adult C. elegans increased life span and, conversely, inhibition of vrk-1 decreased life span. In addition, vrk-1 was required for longevity conferred by mutations that inhibit C. elegans mitochondrial respiration, which requires AMPK. VRK-1 directly phosphorylated and up-regulated AMPK in both C. elegans and cultured human cells. Thus, our data show that the somatic nuclear kinase, VRK-1, promotes longevity through AMPK activation, and this function appears to be conserved between C. elegans and humans. acknowledgement: 'This research was supported by grants NRF-2019R1A3B2067745 and NRF-2017R1A5A1015366 funded by the Korean Government (MSIT) through the National Research Foundation (NRF) of Korea to S.-J.V.L. and by grant Basic Science Research Program (No. 2019R1A2C2009440) funded by the Korean Government (MSIT) through the NRF of Korea to K.-T.K. ' article_number: aaw7824 article_processing_charge: No article_type: original author: - first_name: Sangsoon full_name: Park, Sangsoon last_name: Park - first_name: Murat full_name: Artan, Murat id: C407B586-6052-11E9-B3AE-7006E6697425 last_name: Artan orcid: 0000-0001-8945-6992 - first_name: Seung Hyun full_name: Han, Seung Hyun last_name: Han - first_name: Hae-Eun H. full_name: Park, Hae-Eun H. last_name: Park - first_name: Yoonji full_name: Jung, Yoonji last_name: Jung - first_name: Ara B. full_name: Hwang, Ara B. last_name: Hwang - first_name: Won Sik full_name: Shin, Won Sik last_name: Shin - first_name: Kyong-Tai full_name: Kim, Kyong-Tai last_name: Kim - first_name: Seung-Jae V. full_name: Lee, Seung-Jae V. last_name: Lee citation: ama: Park S, Artan M, Han SH, et al. VRK-1 extends life span by activation of AMPK via phosphorylation. Science Advances. 2020;6(27). doi:10.1126/sciadv.aaw7824 apa: Park, S., Artan, M., Han, S. H., Park, H.-E. H., Jung, Y., Hwang, A. B., … Lee, S.-J. V. (2020). VRK-1 extends life span by activation of AMPK via phosphorylation. Science Advances. American Association for the Advancement of Science. https://doi.org/10.1126/sciadv.aaw7824 chicago: Park, Sangsoon, Murat Artan, Seung Hyun Han, Hae-Eun H. Park, Yoonji Jung, Ara B. Hwang, Won Sik Shin, Kyong-Tai Kim, and Seung-Jae V. Lee. “VRK-1 Extends Life Span by Activation of AMPK via Phosphorylation.” Science Advances. American Association for the Advancement of Science, 2020. https://doi.org/10.1126/sciadv.aaw7824. ieee: S. Park et al., “VRK-1 extends life span by activation of AMPK via phosphorylation,” Science Advances, vol. 6, no. 27. American Association for the Advancement of Science, 2020. ista: Park S, Artan M, Han SH, Park H-EH, Jung Y, Hwang AB, Shin WS, Kim K-T, Lee S-JV. 2020. VRK-1 extends life span by activation of AMPK via phosphorylation. Science Advances. 6(27), aaw7824. mla: Park, Sangsoon, et al. “VRK-1 Extends Life Span by Activation of AMPK via Phosphorylation.” Science Advances, vol. 6, no. 27, aaw7824, American Association for the Advancement of Science, 2020, doi:10.1126/sciadv.aaw7824. short: S. Park, M. Artan, S.H. Han, H.-E.H. Park, Y. Jung, A.B. Hwang, W.S. Shin, K.-T. Kim, S.-J.V. Lee, Science Advances 6 (2020). date_created: 2024-03-04T09:41:57Z date_published: 2020-07-01T00:00:00Z date_updated: 2024-03-04T09:52:09Z day: '01' ddc: - '570' department: - _id: MaDe doi: 10.1126/sciadv.aaw7824 file: - access_level: open_access checksum: a37157cd0de709dce5fe03f4a31cd0b6 content_type: application/pdf creator: dernst date_created: 2024-03-04T09:46:41Z date_updated: 2024-03-04T09:46:41Z file_id: '15058' file_name: 2020_ScienceAdvances_Park.pdf file_size: 1864415 relation: main_file success: 1 file_date_updated: 2024-03-04T09:46:41Z has_accepted_license: '1' intvolume: ' 6' issue: '27' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '07' oa: 1 oa_version: Published Version publication: Science Advances publication_identifier: eissn: - 2375-2548 publication_status: published publisher: American Association for the Advancement of Science quality_controlled: '1' status: public title: VRK-1 extends life span by activation of AMPK via phosphorylation tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2020' ... --- _id: '7340' abstract: - lang: eng text: Coupling of endoplasmic reticulum stress to dimerisation‑dependent activation of the UPR transducer IRE1 is incompletely understood. Whilst the luminal co-chaperone ERdj4 promotes a complex between the Hsp70 BiP and IRE1's stress-sensing luminal domain (IRE1LD) that favours the latter's monomeric inactive state and loss of ERdj4 de-represses IRE1, evidence linking these cellular and in vitro observations is presently lacking. We report that enforced loading of endogenous BiP onto endogenous IRE1α repressed UPR signalling in CHO cells and deletions in the IRE1α locus that de-repressed the UPR in cells, encode flexible regions of IRE1LD that mediated BiP‑induced monomerisation in vitro. Changes in the hydrogen exchange mass spectrometry profile of IRE1LD induced by ERdj4 and BiP confirmed monomerisation and were consistent with active destabilisation of the IRE1LD dimer. Together, these observations support a competition model whereby waning ER stress passively partitions ERdj4 and BiP to IRE1LD to initiate active repression of UPR signalling. acknowledgement: We thank the CIMR flow cytometry core facility team (Reiner Schulte, Chiara Cossetti and Gabriela Grondys-Kotarba) for assistance with FACS, the Huntington lab for access to the Octet machine, Steffen Preissler for advice on data interpretation, Roman Kityk and Nicole Luebbehusen for help and advice with HX-MS experiments. article_number: e50793 article_processing_charge: No article_type: original author: - first_name: Niko Paresh full_name: Amin-Wetzel, Niko Paresh id: E95D3014-9D8C-11E9-9C80-D2F8E5697425 last_name: Amin-Wetzel - first_name: Lisa full_name: Neidhardt, Lisa last_name: Neidhardt - first_name: Yahui full_name: Yan, Yahui last_name: Yan - first_name: Matthias P. full_name: Mayer, Matthias P. last_name: Mayer - first_name: David full_name: Ron, David last_name: Ron citation: ama: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR. eLife. 2019;8. doi:10.7554/eLife.50793 apa: Amin-Wetzel, N. P., Neidhardt, L., Yan, Y., Mayer, M. P., & Ron, D. (2019). Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.50793 chicago: Amin-Wetzel, Niko Paresh, Lisa Neidhardt, Yahui Yan, Matthias P. Mayer, and David Ron. “Unstructured Regions in IRE1α Specify BiP-Mediated Destabilisation of the Luminal Domain Dimer and Repression of the UPR.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.50793. ieee: N. P. Amin-Wetzel, L. Neidhardt, Y. Yan, M. P. Mayer, and D. Ron, “Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR,” eLife, vol. 8. eLife Sciences Publications, 2019. ista: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. 2019. Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR. eLife. 8, e50793. mla: Amin-Wetzel, Niko Paresh, et al. “Unstructured Regions in IRE1α Specify BiP-Mediated Destabilisation of the Luminal Domain Dimer and Repression of the UPR.” ELife, vol. 8, e50793, eLife Sciences Publications, 2019, doi:10.7554/eLife.50793. short: N.P. Amin-Wetzel, L. Neidhardt, Y. Yan, M.P. Mayer, D. Ron, ELife 8 (2019). date_created: 2020-01-19T23:00:39Z date_published: 2019-12-24T00:00:00Z date_updated: 2023-09-06T14:58:02Z day: '24' ddc: - '570' department: - _id: MaDe doi: 10.7554/eLife.50793 external_id: isi: - '000512303700001' pmid: - '31873072' file: - access_level: open_access checksum: 29fcbcd8c1fc7f11a596ed7f14ea1c82 content_type: application/pdf creator: dernst date_created: 2020-11-19T11:37:41Z date_updated: 2020-11-19T11:37:41Z file_id: '8777' file_name: 2019_eLife_AminWetzel.pdf file_size: 4817384 relation: main_file success: 1 file_date_updated: 2020-11-19T11:37:41Z has_accepted_license: '1' intvolume: ' 8' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 8 year: '2019' ...