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dc.contributor.authorGiese, Gabrielle E.
dc.contributor.authorWalker, Melissa D.
dc.contributor.authorPonomarova, Olga
dc.contributor.authorZhang, Hefei
dc.contributor.authorLi, Xuhang
dc.contributor.authorMinevich, Gregory
dc.contributor.authorWalhout, Albertha J. M.
dc.date2022-08-11T08:09:57.000
dc.date.accessioned2022-08-23T16:50:12Z
dc.date.available2022-08-23T16:50:12Z
dc.date.issued2020-10-05
dc.date.submitted2020-12-03
dc.identifier.citation<p>Giese GE, Walker MD, Ponomarova O, Zhang H, Li X, Minevich G, Walhout AJ. <em>Caenorhabditis elegans</em> methionine/S-adenosylmethionine cycle activity is sensed and adjusted by a nuclear hormone receptor. Elife. 2020 Oct 5;9:e60259. doi: 10.7554/eLife.60259. PMID: 33016879; PMCID: PMC7561351. <a href="https://doi.org/10.7554/eLife.60259">Link to article on publisher's site</a></p>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.60259
dc.identifier.pmid33016879
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41614
dc.description.abstractVitamin B12 is an essential micronutrient that functions in two metabolic pathways: the canonical propionate breakdown pathway and the methionine/S-adenosylmethionine (Met/SAM) cycle. In Caenorhabditis elegans, low vitamin B12, or genetic perturbation of the canonical propionate breakdown pathway results in propionate accumulation and the transcriptional activation of a propionate shunt pathway. This propionate-dependent mechanism requires nhr-10 and is referred to as 'B12-mechanism-I'. Here, we report that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanism we refer to as 'B12-mechanism-II'. This mechanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin B12. B12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transporter, pmp-5, and adjust influx and efflux of the cycle by activating msra-1 and repressing cbs-1, respectively. Taken together, Met/SAM cycle activity is sensed and transcriptionally adjusted to be in a tight metabolic regime.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=33016879&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2020, Giese et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectC. elegans
dc.subjectchromosomes
dc.subjectcomputational biology
dc.subjectgene expression
dc.subjectmetabolism
dc.subjectmethionine/sam cycle
dc.subjectnuclear hormone receptor
dc.subjectsystems biology
dc.subjecttranscription factors
dc.subjectvitamin B12
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBiochemistry
dc.subjectCellular and Molecular Physiology
dc.subjectComputational Biology
dc.subjectHormones, Hormone Substitutes, and Hormone Antagonists
dc.subjectSystems Biology
dc.titleCaenorhabditis elegans methionine/S-adenosylmethionine cycle activity is sensed and adjusted by a nuclear hormone receptor
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5431&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4401
dc.identifier.contextkey20386585
refterms.dateFOA2022-08-23T16:50:12Z
html.description.abstract<p>Vitamin B12 is an essential micronutrient that functions in two metabolic pathways: the canonical propionate breakdown pathway and the methionine/S-adenosylmethionine (Met/SAM) cycle. In Caenorhabditis elegans, low vitamin B12, or genetic perturbation of the canonical propionate breakdown pathway results in propionate accumulation and the transcriptional activation of a propionate shunt pathway. This propionate-dependent mechanism requires nhr-10 and is referred to as 'B12-mechanism-I'. Here, we report that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanism we refer to as 'B12-mechanism-II'. This mechanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin B12. B12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transporter, pmp-5, and adjust influx and efflux of the cycle by activating msra-1 and repressing cbs-1, respectively. Taken together, Met/SAM cycle activity is sensed and transcriptionally adjusted to be in a tight metabolic regime.</p>
dc.identifier.submissionpathoapubs/4401
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentProgram in Systems Biology
dc.source.pagese60259


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Copyright © 2020, Giese et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright © 2020, Giese et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.