[{"department":[{"_id":"LoSw"},{"_id":"MaDe"},{"_id":"GaNo"}],"author":[{"last_name":"Jaeger","first_name":"Eliza C.B.","full_name":"Jaeger, Eliza C.B."},{"first_name":"David","full_name":"Vijatovic, David","id":"cf391e77-ec3c-11ea-a124-d69323410b58","last_name":"Vijatovic"},{"last_name":"Deryckere","first_name":"Astrid","full_name":"Deryckere, Astrid"},{"last_name":"Zorin","first_name":"Nikol","full_name":"Zorin, Nikol"},{"last_name":"Nguyen","full_name":"Nguyen, Akemi L.","first_name":"Akemi L."},{"first_name":"Georgiy","full_name":"Ivanian, Georgiy","id":"eaf2b366-cfd1-11ee-bbdf-c8790f800a05","last_name":"Ivanian"},{"last_name":"Woych","first_name":"Jamie","full_name":"Woych, Jamie"},{"full_name":"Arnold, Rebecca C","first_name":"Rebecca C","last_name":"Arnold","id":"d6cce458-14c9-11ed-a755-c1c8fc6fde6f"},{"full_name":"Ortega Gurrola, Alonso","first_name":"Alonso","last_name":"Ortega Gurrola"},{"first_name":"Arik","full_name":"Shvartsman, Arik","last_name":"Shvartsman"},{"last_name":"Barbieri","id":"a9492887-8972-11ed-ae7b-bfae10998254","full_name":"Barbieri, Francesca","first_name":"Francesca"},{"id":"85dd99f2-15b2-11ec-abd3-d1ae4d57f3b5","last_name":"Toma","first_name":"Florina-Alexandra","full_name":"Toma, Florina-Alexandra"},{"first_name":"Gary J.","full_name":"Gorbsky, Gary J.","last_name":"Gorbsky"},{"last_name":"Horb","full_name":"Horb, Marko E.","first_name":"Marko E."},{"last_name":"Cline","first_name":"Hollis T.","full_name":"Cline, Hollis T."},{"last_name":"Shay","full_name":"Shay, Timothy F.","first_name":"Timothy F."},{"last_name":"Kelley","full_name":"Kelley, Darcy B.","first_name":"Darcy B."},{"last_name":"Yamaguchi","first_name":"Ayako","full_name":"Yamaguchi, Ayako"},{"last_name":"Shein-Idelson","full_name":"Shein-Idelson, Mark","first_name":"Mark"},{"last_name":"Tosches","full_name":"Tosches, Maria Antonietta","first_name":"Maria Antonietta"},{"id":"56BE8254-C4F0-11E9-8E45-0B23E6697425","last_name":"Sweeney","orcid":"0000-0001-9242-5601","first_name":"Lora Beatrice Jaeger","full_name":"Sweeney, Lora Beatrice Jaeger"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Adeno-associated viral tools to trace neural development and connectivity across amphibians","_id":"15016","language":[{"iso":"eng"}],"year":"2024","day":"16","status":"public","month":"02","oa_version":"Preprint","date_created":"2024-02-20T09:20:32Z","publication":"bioRxiv","date_published":"2024-02-16T00:00:00Z","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","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.).","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.","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.","ieee":"E. C. B. Jaeger et al., “Adeno-associated viral tools to trace neural development and connectivity across amphibians,” bioRxiv. ."},"date_updated":"2024-02-20T09:34:25Z","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2024.02.15.580289"}],"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","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. "}],"type":"preprint","doi":"10.1101/2024.02.15.580289","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"},{"name":"Development and Evolution of Tetrapod Motor Circuits","grant_number":"101041551","_id":"ebb66355-77a9-11ec-83b8-b8ac210a4dae"}],"oa":1,"publication_status":"submitted"},{"department":[{"_id":"MaDe"}],"volume":181,"editor":[{"last_name":"Yamamoto","first_name":"Daisuke","full_name":"Yamamoto, Daisuke"}],"author":[{"first_name":"Murat","full_name":"Artan, Murat","id":"C407B586-6052-11E9-B3AE-7006E6697425","last_name":"Artan"},{"last_name":"de Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","full_name":"de Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443"}],"status":"public","day":"04","language":[{"iso":"eng"}],"year":"2022","scopus_import":"1","oa_version":"None","intvolume":" 181","month":"06","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","short":"M. Artan, M. de Bono, in:, D. Yamamoto (Ed.), Behavioral Neurogenetics, Springer Nature, New York, 2022, pp. 277–294.","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.","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.","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.","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."},"publication":"Behavioral Neurogenetics","date_published":"2022-06-04T00:00:00Z","article_processing_charge":"No","type":"book_chapter","doi":"10.1007/978-1-0716-2321-3_15","series_title":"NM","publication_status":"published","page":"277-294","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Proteomic Analysis of C. Elegans Neurons Using TurboID-Based Proximity Labeling","quality_controlled":"1","_id":"11456","alternative_title":["Neuromethods"],"date_created":"2022-06-20T08:10:34Z","publisher":"Springer Nature","date_updated":"2023-02-21T09:51:55Z","place":"New York","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).","publication_identifier":{"isbn":["9781071623206"],"eisbn":["9781071623213"],"issn":["0893-2336"],"eissn":["1940-6045"]},"ec_funded":1,"abstract":[{"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.","lang":"eng"}],"project":[{"grant_number":"209504/A/17/Z","name":"Molecular mechanisms of neural circuit function","_id":"23870BE8-32DE-11EA-91FC-C7463DDC885E"},{"name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425"}]},{"status":"public","language":[{"iso":"eng"}],"year":"2022","day":"24","has_accepted_license":"1","article_type":"original","author":[{"last_name":"Valperga","id":"67F289DE-0D8F-11EA-9BDD-54AE3DDC885E","full_name":"Valperga, Giulio","first_name":"Giulio"},{"full_name":"De Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443","last_name":"De Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"}],"article_number":"e68040","pmid":1,"department":[{"_id":"MaDe"}],"volume":11,"publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"ScienComp"}],"article_processing_charge":"No","doi":"10.7554/eLife.68040","type":"journal_article","oa_version":"Published Version","scopus_import":"1","month":"02","file_date_updated":"2022-03-07T07:39:25Z","intvolume":" 11","citation":{"short":"G. Valperga, M. de Bono, ELife 11 (2022).","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.","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.","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."},"publication":"eLife","date_published":"2022-02-24T00:00:00Z","_id":"10826","quality_controlled":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans","isi":1,"file":[{"relation":"main_file","date_updated":"2022-03-07T07:39:25Z","creator":"dernst","file_id":"10830","date_created":"2022-03-07T07:39:25Z","checksum":"cc1b9bf866d0f61f965556e0dd03d3ac","file_size":4095591,"success":1,"access_level":"open_access","content_type":"application/pdf","file_name":"2022_eLife_Valperga.pdf"}],"oa":1,"project":[{"_id":"23870BE8-32DE-11EA-91FC-C7463DDC885E","grant_number":"209504/A/17/Z","name":"Molecular mechanisms of neural circuit function"}],"publication_identifier":{"eissn":["2050084X"]},"ddc":["570"],"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."}],"date_updated":"2023-08-02T14:42:55Z","external_id":{"pmid":["35201977"],"isi":["000763432300001"]},"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).","date_created":"2022-03-06T23:01:52Z","publisher":"eLife Sciences Publications"},{"external_id":{"pmid":["35727855"],"isi":["000828679600001"]},"date_updated":"2023-08-03T12:11:44Z","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.","publisher":"Public Library of Science","date_created":"2022-07-24T22:01:42Z","oa":1,"project":[{"grant_number":"209504/A/17/Z","name":"Molecular mechanisms of neural circuit function","_id":"23870BE8-32DE-11EA-91FC-C7463DDC885E"}],"issue":"6","publication_identifier":{"eissn":["1545-7885"]},"ddc":["570"],"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."}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis elegans","file":[{"file_size":3721585,"checksum":"df4902f854ad76769d3203bfdc69f16c","date_created":"2022-07-25T07:38:49Z","file_id":"11643","creator":"dernst","date_updated":"2022-07-25T07:38:49Z","relation":"main_file","file_name":"2022_PLoSBiology_Zhao.pdf","content_type":"application/pdf","access_level":"open_access","success":1}],"isi":1,"_id":"11637","quality_controlled":"1","intvolume":" 20","month":"06","file_date_updated":"2022-07-25T07:38:49Z","scopus_import":"1","oa_version":"Published Version","publication":"PLoS Biology","date_published":"2022-06-21T00:00:00Z","citation":{"short":"L. Zhao, L.A. Fenk, L. Nilsson, N.P. Amin-Wetzel, N. Ramirez, M. de Bono, C. Chen, PLoS Biology 20 (2022).","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","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","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.","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.","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."},"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","article_processing_charge":"No","type":"journal_article","doi":"10.1371/journal.pbio.3001684","author":[{"full_name":"Zhao, Lina","first_name":"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"},{"id":"E95D3014-9D8C-11E9-9C80-D2F8E5697425","last_name":"Amin-Wetzel","first_name":"Niko Paresh","full_name":"Amin-Wetzel, Niko Paresh"},{"id":"39831956-E4FE-11E9-85DE-0DC7E5697425","last_name":"Ramirez","first_name":"Nelson","full_name":"Ramirez, Nelson"},{"full_name":"De Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443","last_name":"De Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Chen, Changchun","first_name":"Changchun","last_name":"Chen"}],"article_number":"e3001684","department":[{"_id":"MaDe"}],"pmid":1,"volume":20,"day":"21","year":"2022","language":[{"iso":"eng"}],"status":"public","has_accepted_license":"1","article_type":"original"},{"date_created":"2022-09-11T22:01:55Z","publisher":"Elsevier","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).","date_updated":"2023-08-03T13:56:46Z","external_id":{"isi":["000884241800011"],"pmid":["35933017"]},"ec_funded":1,"ddc":["570"],"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."}],"publication_identifier":{"issn":["0021-9258"],"eissn":["1083-351X"]},"issue":"9","project":[{"name":"Molecular mechanisms of neural circuit function","grant_number":"209504/A/17/Z","_id":"23870BE8-32DE-11EA-91FC-C7463DDC885E"},{"grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425"}],"oa":1,"isi":1,"file":[{"success":1,"access_level":"open_access","content_type":"application/pdf","file_name":"2022_JBC_Artan.pdf","relation":"main_file","date_updated":"2022-09-12T08:14:50Z","file_id":"12092","creator":"dernst","file_size":2101656,"date_created":"2022-09-12T08:14:50Z","checksum":"e726c7b9315230e6710e0b1f1d1677e9"}],"title":"Depletion of endogenously biotinylated carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in Caenorhabditis elegans","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","quality_controlled":"1","_id":"12082","citation":{"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.","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.","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).","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","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","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."},"publication":"Journal of Biological Chemistry","date_published":"2022-09-01T00:00:00Z","oa_version":"Published Version","scopus_import":"1","intvolume":" 298","month":"09","file_date_updated":"2022-09-12T08:14:50Z","doi":"10.1016/j.jbc.2022.102343","type":"journal_article","article_processing_charge":"No","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"Bio"}],"volume":298,"pmid":1,"department":[{"_id":"MaDe"}],"article_number":"102343","author":[{"last_name":"Artan","id":"C407B586-6052-11E9-B3AE-7006E6697425","full_name":"Artan, Murat","first_name":"Murat"},{"last_name":"Hartl","first_name":"Markus","full_name":"Hartl, Markus"},{"full_name":"Chen, Weiqiang","first_name":"Weiqiang","last_name":"Chen"},{"orcid":"0000-0001-8347-0443","first_name":"Mario","full_name":"De Bono, Mario","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","last_name":"De Bono"}],"article_type":"original","has_accepted_license":"1","status":"public","language":[{"iso":"eng"}],"day":"01","year":"2022"},{"quality_controlled":"1","keyword":["Genetics","Molecular Biology","Biochemistry"],"_id":"12275","isi":1,"title":"Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","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."}],"publication_identifier":{"eissn":["1469-3178"],"issn":["1469-221X"]},"issue":"7","oa":1,"date_created":"2023-01-16T10:01:44Z","publisher":"Embo Press","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","main_file_link":[{"open_access":"1","url":"https://doi.org/10.15252/embr.202154163"}],"date_updated":"2023-10-03T11:25:54Z","external_id":{"isi":["000797302700001"],"pmid":["35586945"]},"article_type":"original","has_accepted_license":"1","status":"public","day":"05","year":"2022","language":[{"iso":"eng"}],"volume":23,"department":[{"_id":"MaDe"}],"pmid":1,"article_number":"e54163","author":[{"last_name":"Rahman","first_name":"Maisha","full_name":"Rahman, Maisha"},{"id":"39831956-E4FE-11E9-85DE-0DC7E5697425","last_name":"Ramirez","first_name":"Nelson","full_name":"Ramirez, Nelson"},{"full_name":"Diaz‐Balzac, Carlos A","first_name":"Carlos A","last_name":"Diaz‐Balzac"},{"first_name":"Hannes E","full_name":"Bülow, Hannes E","last_name":"Bülow"}],"type":"journal_article","doi":"10.15252/embr.202154163","article_processing_charge":"No","publication_status":"published","citation":{"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.","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.","short":"M. Rahman, N. Ramirez, C.A. Diaz‐Balzac, H.E. Bülow, EMBO Reports 23 (2022).","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."},"publication":"EMBO Reports","date_published":"2022-07-05T00:00:00Z","oa_version":"Published Version","scopus_import":"1","intvolume":" 23","month":"07"},{"author":[{"id":"C407B586-6052-11E9-B3AE-7006E6697425","last_name":"Artan","orcid":"0000-0001-8945-6992","first_name":"Murat","full_name":"Artan, Murat"},{"last_name":"Sohn","first_name":"Jooyeon","full_name":"Sohn, Jooyeon"},{"first_name":"Cheolju","full_name":"Lee, Cheolju","last_name":"Lee"},{"last_name":"Park","first_name":"Seung Yeol","full_name":"Park, Seung Yeol"},{"last_name":"Lee","first_name":"Seung Jae V.","full_name":"Lee, Seung Jae V."}],"pmid":1,"department":[{"_id":"MaDe"}],"volume":18,"day":"19","year":"2022","language":[{"iso":"eng"}],"status":"public","article_type":"original","month":"02","intvolume":" 18","oa_version":"Published Version","scopus_import":"1","date_published":"2022-02-19T00:00:00Z","publication":"Autophagy","citation":{"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.","short":"M. Artan, J. Sohn, C. Lee, S.Y. Park, S.J.V. Lee, Autophagy 18 (2022) 1208–1210.","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","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.","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.","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."},"page":"1208-1210","publication_status":"published","article_processing_charge":"No","type":"journal_article","doi":"10.1080/15548627.2022.2039523","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications","isi":1,"_id":"10846","quality_controlled":"1","external_id":{"pmid":["35188063"],"isi":["000758859600001"]},"date_updated":"2023-10-03T10:54:54Z","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).","main_file_link":[{"url":"https://doi.org/10.1080/15548627.2022.2039523","open_access":"1"}],"publisher":"Taylor & Francis","date_created":"2022-03-13T23:01:47Z","oa":1,"issue":"5","publication_identifier":{"issn":["1554-8627"],"eissn":["1554-8635"]},"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."}]},{"article_number":"101094","author":[{"first_name":"Murat","full_name":"Artan, Murat","orcid":"0000-0001-8945-6992","id":"C407B586-6052-11E9-B3AE-7006E6697425","last_name":"Artan"},{"last_name":"Barratt","id":"57740d2b-2a88-11ec-97cf-d9e6d1b39677","full_name":"Barratt, Stephen","first_name":"Stephen"},{"last_name":"Flynn","full_name":"Flynn, Sean M.","first_name":"Sean M."},{"first_name":"Farida","full_name":"Begum, Farida","last_name":"Begum"},{"full_name":"Skehel, Mark","first_name":"Mark","last_name":"Skehel"},{"first_name":"Armel","full_name":"Nicolas, Armel","id":"2A103192-F248-11E8-B48F-1D18A9856A87","last_name":"Nicolas"},{"full_name":"De Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443","last_name":"De Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"}],"volume":297,"department":[{"_id":"MaDe"},{"_id":"LifeSc"}],"year":"2021","language":[{"iso":"eng"}],"day":"01","status":"public","article_type":"original","has_accepted_license":"1","date_published":"2021-09-01T00:00:00Z","publication":"Journal of Biological Chemistry","citation":{"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.","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","short":"M. Artan, S. Barratt, S.M. Flynn, F. Begum, M. Skehel, A. Nicolas, M. de Bono, Journal of Biological Chemistry 297 (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.","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.","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."},"month":"09","file_date_updated":"2021-10-11T12:20:58Z","intvolume":" 297","oa_version":"Published Version","scopus_import":"1","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","type":"journal_article","doi":"10.1016/J.JBC.2021.101094","article_processing_charge":"Yes","title":"Interactome analysis of Caenorhabditis elegans synapses by TurboID-based proximity labeling","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","file":[{"date_updated":"2021-10-11T12:20:58Z","relation":"main_file","creator":"cchlebak","file_id":"10121","checksum":"19e39d36c5b9387c6dc0e89c9ae856ab","date_created":"2021-10-11T12:20:58Z","file_size":1680010,"access_level":"open_access","success":1,"content_type":"application/pdf","file_name":"2021_JBC_Artan.pdf"}],"isi":1,"_id":"10117","quality_controlled":"1","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).","external_id":{"isi":["000706409200006"]},"date_updated":"2023-08-14T07:24:09Z","publisher":"Elsevier","date_created":"2021-10-10T22:01:23Z","issue":"3","project":[{"grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425"}],"oa":1,"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."}],"ddc":["612"],"ec_funded":1,"publication_identifier":{"issn":["0021-9258"],"eissn":["1083-351X"]}},{"date_created":"2021-10-10T22:01:22Z","publisher":"eLife Sciences Publications","date_updated":"2023-08-14T07:23:39Z","external_id":{"pmid":["34499028"],"isi":["000695716100001"]},"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).","publication_identifier":{"eissn":["2050-084X"]},"ec_funded":1,"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."}],"ddc":["610"],"project":[{"call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425","name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411"}],"oa":1,"isi":1,"file":[{"date_created":"2021-10-11T14:15:07Z","checksum":"b465e172d2b1f57aa26a2571a085d052","file_size":1774624,"creator":"cchlebak","file_id":"10122","date_updated":"2021-10-11T14:15:07Z","relation":"main_file","file_name":"2021_eLife_VuongBrender.pdf","content_type":"application/pdf","access_level":"open_access","success":1}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Neuronal calmodulin levels are controlled by CAMTA transcription factors","quality_controlled":"1","_id":"10116","scopus_import":"1","oa_version":"Published Version","month":"09","intvolume":" 10","file_date_updated":"2021-10-11T14:15:07Z","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","short":"T. Vuong-Brender, S. Flynn, Y. Vallis, M. de Bono, ELife 10 (2021).","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.","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.","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."},"publication":"eLife","date_published":"2021-09-17T00:00:00Z","article_processing_charge":"No","type":"journal_article","doi":"10.7554/eLife.68238","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"pmid":1,"department":[{"_id":"MaDe"}],"volume":10,"author":[{"last_name":"Vuong-Brender","id":"D389312E-10C4-11EA-ABF4-A4B43DDC885E","full_name":"Vuong-Brender, Thanh","first_name":"Thanh"},{"first_name":"Sean","full_name":"Flynn, Sean","last_name":"Flynn"},{"id":"05A2795C-31B5-11EA-83A7-7DA23DDC885E","last_name":"Vallis","first_name":"Yvonne","full_name":"Vallis, Yvonne"},{"full_name":"De Bono, Mario","first_name":"Mario","orcid":"0000-0001-8347-0443","last_name":"De Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"}],"article_number":"e68238","has_accepted_license":"1","article_type":"original","status":"public","day":"17","year":"2021","language":[{"iso":"eng"}]},{"has_accepted_license":"1","article_type":"original","status":"public","year":"2021","day":"01","language":[{"iso":"eng"}],"pmid":1,"department":[{"_id":"MaDe"}],"volume":19,"author":[{"last_name":"Chauve","first_name":"Laetitia","full_name":"Chauve, Laetitia"},{"last_name":"Hodge","full_name":"Hodge, Francesca","first_name":"Francesca"},{"last_name":"Murdoch","first_name":"Sharlene","full_name":"Murdoch, Sharlene"},{"last_name":"Masoudzadeh","full_name":"Masoudzadeh, Fatemah","first_name":"Fatemah"},{"last_name":"Mann","first_name":"Harry Jack","full_name":"Mann, Harry Jack"},{"last_name":"Lopez-Clavijo","first_name":"Andrea","full_name":"Lopez-Clavijo, Andrea"},{"full_name":"Okkenhaug, Hanneke","first_name":"Hanneke","last_name":"Okkenhaug"},{"last_name":"West","first_name":"Greg","full_name":"West, Greg"},{"full_name":"Sousa, Bebiana C.","first_name":"Bebiana C.","last_name":"Sousa"},{"last_name":"Segonds-Pichon","full_name":"Segonds-Pichon, Anne","first_name":"Anne"},{"first_name":"Cheryl","full_name":"Li, Cheryl","last_name":"Li"},{"last_name":"Wingett","first_name":"Steven","full_name":"Wingett, Steven"},{"last_name":"Kienberger","full_name":"Kienberger, Hermine","first_name":"Hermine"},{"last_name":"Kleigrewe","first_name":"Karin","full_name":"Kleigrewe, Karin"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","last_name":"De Bono","first_name":"Mario","full_name":"De Bono, Mario","orcid":"0000-0001-8347-0443"},{"first_name":"Michael","full_name":"Wakelam, Michael","last_name":"Wakelam"},{"last_name":"Casanueva","first_name":"Olivia","full_name":"Casanueva, Olivia"}],"article_number":"e3001431","article_processing_charge":"No","type":"journal_article","doi":"10.1371/journal.pbio.3001431","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa_version":"Published Version","scopus_import":"1","month":"11","intvolume":" 19","file_date_updated":"2021-11-22T09:34:03Z","citation":{"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.","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.","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.","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.","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","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","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_published":"2021-11-01T00:00:00Z","publication":"PLoS Biology","quality_controlled":"1","_id":"10322","isi":1,"file":[{"success":1,"access_level":"open_access","content_type":"application/pdf","file_name":"2021_PLoSBio_Chauve.pdf","date_updated":"2021-11-22T09:34:03Z","relation":"main_file","creator":"cchlebak","file_id":"10330","date_created":"2021-11-22T09:34:03Z","checksum":"0c61b667f814fd9435b3ac42036fc36d","file_size":4069215}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues to enable adaptation to high temperatures in C. elegans","publication_identifier":{"eissn":["1545-7885"],"issn":["1544-9173"]},"abstract":[{"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.","lang":"eng"}],"ddc":["570"],"oa":1,"related_material":{"record":[{"status":"public","relation":"research_data","id":"13069"}]},"issue":"11","date_created":"2021-11-21T23:01:28Z","publisher":"Public Library of Science","date_updated":"2023-08-14T11:53:27Z","external_id":{"pmid":["34723964"],"isi":["000715818400001"]},"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."},{"_id":"13069","year":"2021","day":"25","status":"public","author":[{"last_name":"Chauve","full_name":"Chauve, Laetitia","first_name":"Laetitia"},{"first_name":"Francesca","full_name":"Hodge, Francesca","last_name":"Hodge"},{"full_name":"Murdoch, Sharlene","first_name":"Sharlene","last_name":"Murdoch"},{"full_name":"Masoudzadeh, Fatemah","first_name":"Fatemah","last_name":"Masoudzadeh"},{"last_name":"Mann","full_name":"Mann, Harry-Jack","first_name":"Harry-Jack"},{"first_name":"Andrea","full_name":"Lopez-Clavijo, Andrea","last_name":"Lopez-Clavijo"},{"first_name":"Hanneke","full_name":"Okkenhaug, Hanneke","last_name":"Okkenhaug"},{"full_name":"West, Greg","first_name":"Greg","last_name":"West"},{"first_name":"Bebiana C.","full_name":"Sousa, Bebiana C.","last_name":"Sousa"},{"full_name":"Segonds-Pichon, Anne","first_name":"Anne","last_name":"Segonds-Pichon"},{"first_name":"Cheryl","full_name":"Li, Cheryl","last_name":"Li"},{"full_name":"Wingett, Steven","first_name":"Steven","last_name":"Wingett"},{"full_name":"Kienberger, Hermine","first_name":"Hermine","last_name":"Kienberger"},{"last_name":"Kleigrewe","first_name":"Karin","full_name":"Kleigrewe, Karin"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","last_name":"de Bono","orcid":"0000-0001-8347-0443","first_name":"Mario","full_name":"de Bono, Mario"},{"last_name":"Wakelam","full_name":"Wakelam, Michael","first_name":"Michael"},{"first_name":"Olivia","full_name":"Casanueva, Olivia","last_name":"Casanueva"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues to enable adaptation to high temperatures in C. elegans","department":[{"_id":"MaDe"}],"oa":1,"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"related_material":{"record":[{"id":"10322","relation":"used_in_publication","status":"public"}]},"article_processing_charge":"No","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."}],"ddc":["570"],"type":"research_data_reference","doi":"10.5281/ZENODO.5519410","date_updated":"2023-08-14T11:53:26Z","main_file_link":[{"url":"https://doi.org/10.5281/zenodo.5547464","open_access":"1"}],"publisher":"Zenodo","month":"12","oa_version":"Published Version","date_created":"2023-05-23T16:40:56Z","date_published":"2021-12-25T00:00:00Z","citation":{"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.","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","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","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).","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.","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."}},{"pmid":1,"department":[{"_id":"MaDe"}],"volume":105,"author":[{"full_name":"Beets, Isabel","first_name":"Isabel","last_name":"Beets"},{"full_name":"Zhang, Gaotian","first_name":"Gaotian","last_name":"Zhang"},{"last_name":"Fenk","first_name":"Lorenz A.","full_name":"Fenk, Lorenz A."},{"full_name":"Chen, Changchun","first_name":"Changchun","last_name":"Chen"},{"last_name":"Nelson","first_name":"Geoffrey M.","full_name":"Nelson, Geoffrey M."},{"last_name":"Félix","first_name":"Marie-Anne","full_name":"Félix, Marie-Anne"},{"orcid":"0000-0001-8347-0443","first_name":"Mario","full_name":"de Bono, Mario","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","last_name":"de Bono"}],"has_accepted_license":"1","article_type":"original","status":"public","language":[{"iso":"eng"}],"day":"08","year":"2020","oa_version":"Published Version","file_date_updated":"2020-07-14T12:48:00Z","intvolume":" 105","month":"01","citation":{"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.","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.","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.","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","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","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.","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."},"date_published":"2020-01-08T00:00:00Z","publication":"Neuron","article_processing_charge":"No","doi":"10.1016/j.neuron.2019.10.001","type":"journal_article","publication_status":"published","page":"106-121.e10","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"isi":1,"file":[{"relation":"main_file","date_updated":"2020-07-14T12:48:00Z","creator":"dernst","file_id":"7558","date_created":"2020-03-02T15:43:57Z","checksum":"799bfd297a008753a688b30d3958fa48","file_size":3294066,"access_level":"open_access","content_type":"application/pdf","file_name":"2020_Neuron_Beets.pdf"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Natural variation in a dendritic scaffold protein remodels experience-dependent plasticity by altering neuropeptide expression","quality_controlled":"1","_id":"7546","date_created":"2020-02-28T10:43:39Z","publisher":"Cell Press","date_updated":"2023-08-18T06:46:23Z","external_id":{"isi":["000507341300012"],"pmid":["31757604"]},"publication_identifier":{"issn":["0896-6273"]},"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."}],"ddc":["570"],"oa":1,"issue":"1"},{"author":[{"last_name":"Flynn","full_name":"Flynn, Sean M.","first_name":"Sean M."},{"last_name":"Chen","full_name":"Chen, Changchun","first_name":"Changchun"},{"first_name":"Murat","full_name":"Artan, Murat","orcid":"0000-0001-8945-6992","id":"C407B586-6052-11E9-B3AE-7006E6697425","last_name":"Artan"},{"last_name":"Barratt","full_name":"Barratt, Stephen","first_name":"Stephen"},{"last_name":"Crisp","first_name":"Alastair","full_name":"Crisp, Alastair"},{"last_name":"Nelson","full_name":"Nelson, Geoffrey M.","first_name":"Geoffrey M."},{"last_name":"Peak-Chew","full_name":"Peak-Chew, Sew Yeu","first_name":"Sew Yeu"},{"full_name":"Begum, Farida","first_name":"Farida","last_name":"Begum"},{"last_name":"Skehel","full_name":"Skehel, Mark","first_name":"Mark"},{"orcid":"0000-0001-8347-0443","full_name":"De Bono, Mario","first_name":"Mario","last_name":"De Bono","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"}],"article_number":"2099","department":[{"_id":"MaDe"}],"volume":11,"status":"public","year":"2020","language":[{"iso":"eng"}],"day":"29","has_accepted_license":"1","article_type":"original","scopus_import":"1","oa_version":"Published Version","month":"04","intvolume":" 11","file_date_updated":"2020-07-14T12:48:03Z","citation":{"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.","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.","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.","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).","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","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","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."},"publication":"Nature Communications","date_published":"2020-04-29T00:00:00Z","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"article_processing_charge":"No","doi":"10.1038/s41467-020-15872-y","type":"journal_article","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity and longevity","isi":1,"file":[{"file_name":"2020_NatureComm_Flynn.pdf","access_level":"open_access","content_type":"application/pdf","file_size":4609120,"date_created":"2020-05-11T10:36:33Z","checksum":"dce367abf2c1a1d15f58fe6f7de82893","relation":"main_file","date_updated":"2020-07-14T12:48:03Z","file_id":"7817","creator":"dernst"}],"_id":"7804","quality_controlled":"1","date_updated":"2023-08-21T06:21:14Z","external_id":{"isi":["000531855500029"]},"date_created":"2020-05-10T22:00:47Z","publisher":"Springer Nature","oa":1,"publication_identifier":{"eissn":["20411723"]},"abstract":[{"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.","lang":"eng"}],"ddc":["570"]},{"oa":1,"issue":"27","publication_identifier":{"eissn":["2375-2548"]},"ddc":["570"],"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."}],"date_updated":"2024-03-04T09:52:09Z","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. ","publisher":"American Association for the Advancement of Science","date_created":"2024-03-04T09:41:57Z","_id":"15057","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"VRK-1 extends life span by activation of AMPK via phosphorylation","file":[{"file_size":1864415,"checksum":"a37157cd0de709dce5fe03f4a31cd0b6","date_created":"2024-03-04T09:46:41Z","relation":"main_file","date_updated":"2024-03-04T09:46:41Z","file_id":"15058","creator":"dernst","file_name":"2020_ScienceAdvances_Park.pdf","access_level":"open_access","success":1,"content_type":"application/pdf"}],"tmp":{"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)","image":"/images/cc_by_nc.png"},"publication_status":"published","article_processing_charge":"No","license":"https://creativecommons.org/licenses/by-nc/4.0/","doi":"10.1126/sciadv.aaw7824","type":"journal_article","month":"07","intvolume":" 6","file_date_updated":"2024-03-04T09:46:41Z","oa_version":"Published Version","date_published":"2020-07-01T00:00:00Z","publication":"Science Advances","citation":{"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.","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.","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).","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"},"language":[{"iso":"eng"}],"day":"01","year":"2020","status":"public","has_accepted_license":"1","article_type":"original","author":[{"last_name":"Park","first_name":"Sangsoon","full_name":"Park, Sangsoon"},{"last_name":"Artan","id":"C407B586-6052-11E9-B3AE-7006E6697425","orcid":"0000-0001-8945-6992","full_name":"Artan, Murat","first_name":"Murat"},{"last_name":"Han","first_name":"Seung Hyun","full_name":"Han, Seung Hyun"},{"first_name":"Hae-Eun H.","full_name":"Park, Hae-Eun H.","last_name":"Park"},{"first_name":"Yoonji","full_name":"Jung, Yoonji","last_name":"Jung"},{"full_name":"Hwang, Ara B.","first_name":"Ara B.","last_name":"Hwang"},{"last_name":"Shin","first_name":"Won Sik","full_name":"Shin, Won Sik"},{"first_name":"Kyong-Tai","full_name":"Kim, Kyong-Tai","last_name":"Kim"},{"last_name":"Lee","full_name":"Lee, Seung-Jae V.","first_name":"Seung-Jae V."}],"article_number":"aaw7824","department":[{"_id":"MaDe"}],"volume":6},{"article_type":"original","has_accepted_license":"1","status":"public","year":"2019","language":[{"iso":"eng"}],"day":"24","volume":8,"pmid":1,"department":[{"_id":"MaDe"}],"article_number":"e50793","author":[{"last_name":"Amin-Wetzel","id":"E95D3014-9D8C-11E9-9C80-D2F8E5697425","full_name":"Amin-Wetzel, Niko Paresh","first_name":"Niko Paresh"},{"last_name":"Neidhardt","full_name":"Neidhardt, Lisa","first_name":"Lisa"},{"full_name":"Yan, Yahui","first_name":"Yahui","last_name":"Yan"},{"full_name":"Mayer, Matthias P.","first_name":"Matthias P.","last_name":"Mayer"},{"full_name":"Ron, David","first_name":"David","last_name":"Ron"}],"doi":"10.7554/eLife.50793","type":"journal_article","article_processing_charge":"No","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"citation":{"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.","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.","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.","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","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","short":"N.P. Amin-Wetzel, L. Neidhardt, Y. Yan, M.P. Mayer, D. Ron, ELife 8 (2019).","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."},"publication":"eLife","date_published":"2019-12-24T00:00:00Z","scopus_import":"1","oa_version":"Published Version","file_date_updated":"2020-11-19T11:37:41Z","intvolume":" 8","month":"12","quality_controlled":"1","_id":"7340","isi":1,"file":[{"file_name":"2019_eLife_AminWetzel.pdf","success":1,"access_level":"open_access","content_type":"application/pdf","file_size":4817384,"checksum":"29fcbcd8c1fc7f11a596ed7f14ea1c82","date_created":"2020-11-19T11:37:41Z","date_updated":"2020-11-19T11:37:41Z","relation":"main_file","file_id":"8777","creator":"dernst"}],"title":"Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","ddc":["570"],"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."}],"publication_identifier":{"eissn":["2050084X"]},"oa":1,"date_created":"2020-01-19T23:00:39Z","publisher":"eLife Sciences Publications","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.","date_updated":"2023-09-06T14:58:02Z","external_id":{"isi":["000512303700001"],"pmid":["31873072"]}}]