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dc.contributor.authorDing, Wei
dc.contributor.authorSmulan, Lorissa J.
dc.contributor.authorHou, Nicole S.
dc.contributor.authorTaubert, Stefan
dc.contributor.authorWatts, Jennifer L.
dc.contributor.authorWalker, Amy K
dc.date2022-08-11T08:10:18.000
dc.date.accessioned2022-08-23T17:03:36Z
dc.date.available2022-08-23T17:03:36Z
dc.date.issued2015-10-06
dc.date.submitted2016-04-13
dc.identifier.citationCell Metab. 2015 Oct 6;22(4):633-45. doi: 10.1016/j.cmet.2015.07.013. Epub 2015 Aug 27. <a href="http://dx.doi.org/10.1016/j.cmet.2015.07.013">Link to article on publisher's site</a>
dc.identifier.issn1550-4131 (Linking)
dc.identifier.doi10.1016/j.cmet.2015.07.013
dc.identifier.pmid26321661
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44463
dc.description.abstracts-adenosylmethionine (SAM) is the sole methyl donor modifying histones, nucleic acids, and phospholipids. Its fluctuation affects hepatic phosphatidylcholine (PC) synthesis or may be linked to variations in DNA or histone methylation. Physiologically, low SAM is associated with lipid accumulation, tissue injury, and immune responses in fatty liver disease. However, molecular connections among SAM limitation, methyltransferases, and disease-associated phenotypes are unclear. We find that low SAM can activate or attenuate Caenorhabditis elegans immune responses. Immune pathways are stimulated downstream of PC production on a non-pathogenic diet. In contrast, distinct SAM-dependent mechanisms limit survival on pathogenic Pseudomonas aeruginosa. C. elegans undertakes a broad transcriptional response to pathogens and we find that low SAM restricts H3K4me3 at Pseudomonas-responsive promoters, limiting their expression. Furthermore, this response depends on the H3K4 methyltransferase set-16/MLL. Thus, our studies provide molecular links between SAM and innate immune functions and suggest that SAM depletion may limit stress-induced gene expression.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26321661&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.cmet.2015.07.013
dc.subjectBiochemistry
dc.subjectCellular and Molecular Physiology
dc.subjectImmunity
dc.subjectMolecular Biology
dc.titles-Adenosylmethionine Levels Govern Innate Immunity through Distinct Methylation-Dependent Pathways
dc.typeJournal Article
dc.source.journaltitleCell metabolism
dc.source.volume22
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/57
dc.identifier.contextkey8471541
html.description.abstract<p>s-adenosylmethionine (SAM) is the sole methyl donor modifying histones, nucleic acids, and phospholipids. Its fluctuation affects hepatic phosphatidylcholine (PC) synthesis or may be linked to variations in DNA or histone methylation. Physiologically, low SAM is associated with lipid accumulation, tissue injury, and immune responses in fatty liver disease. However, molecular connections among SAM limitation, methyltransferases, and disease-associated phenotypes are unclear. We find that low SAM can activate or attenuate Caenorhabditis elegans immune responses. Immune pathways are stimulated downstream of PC production on a non-pathogenic diet. In contrast, distinct SAM-dependent mechanisms limit survival on pathogenic Pseudomonas aeruginosa. C. elegans undertakes a broad transcriptional response to pathogens and we find that low SAM restricts H3K4me3 at Pseudomonas-responsive promoters, limiting their expression. Furthermore, this response depends on the H3K4 methyltransferase set-16/MLL. Thus, our studies provide molecular links between SAM and innate immune functions and suggest that SAM depletion may limit stress-induced gene expression.</p>
dc.identifier.submissionpathpmm_pp/57
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages633-45


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