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dc.contributor.authorVernia, Santiago
dc.contributor.authorEdwards, Yvonne J. K.
dc.contributor.authorHan, Myoung Souk
dc.contributor.authorCavanagh-Kyros, Julie
dc.contributor.authorBarrett, Tamera
dc.contributor.authorKim, Jason K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:19.000
dc.date.accessioned2022-08-23T15:51:05Z
dc.date.available2022-08-23T15:51:05Z
dc.date.issued2016-09-16
dc.date.submitted2016-12-06
dc.identifier.citationElife. 2016 Sep 16;5. pii: e17672. doi: 10.7554/eLife.17672. <a href="http://dx.doi.org/10.7554/eLife.17672">Link to article on publisher's site</a>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.17672
dc.identifier.pmid27635635
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28811
dc.description.abstractAlternative pre-mRNA splicing expands the complexity of the transcriptome and controls isoform-specific gene expression. Whether alternative splicing contributes to metabolic regulation is largely unknown. Here we investigated the contribution of alternative splicing to the development of diet-induced obesity. We found that obesity-induced changes in adipocyte gene expression include alternative pre-mRNA splicing. Bioinformatics analysis associated part of this alternative splicing program with sequence specific NOVA splicing factors. This conclusion was confirmed by studies of mice with NOVA deficiency in adipocytes. Phenotypic analysis of the NOVA-deficient mice demonstrated increased adipose tissue thermogenesis and improved glycemia. We show that NOVA proteins mediate a splicing program that suppresses adipose tissue thermogenesis. Together, these data provide quantitative analysis of gene expression at exon-level resolution in obesity and identify a novel mechanism that contributes to the regulation of adipose tissue function and the maintenance of normal glycemia.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27635635&dopt=Abstract">Link to Article in PubMed</a>
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectJNK
dc.subjectNOVA
dc.subjectadipocyte
dc.subjectcell biology
dc.subjecthigh fat diet
dc.subjecthuman
dc.subjectmouse
dc.subjectpre-mRNA splicing
dc.subjectthermogenesis
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectGenetics and Genomics
dc.titleAn alternative splicing program promotes adipose tissue thermogenesis
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume5
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2053&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1050
dc.identifier.contextkey9445267
refterms.dateFOA2022-08-23T15:51:05Z
html.description.abstract<p>Alternative pre-mRNA splicing expands the complexity of the transcriptome and controls isoform-specific gene expression. Whether alternative splicing contributes to metabolic regulation is largely unknown. Here we investigated the contribution of alternative splicing to the development of diet-induced obesity. We found that obesity-induced changes in adipocyte gene expression include alternative pre-mRNA splicing. Bioinformatics analysis associated part of this alternative splicing program with sequence specific NOVA splicing factors. This conclusion was confirmed by studies of mice with NOVA deficiency in adipocytes. Phenotypic analysis of the NOVA-deficient mice demonstrated increased adipose tissue thermogenesis and improved glycemia. We show that NOVA proteins mediate a splicing program that suppresses adipose tissue thermogenesis. Together, these data provide quantitative analysis of gene expression at exon-level resolution in obesity and identify a novel mechanism that contributes to the regulation of adipose tissue function and the maintenance of normal glycemia.</p>
dc.identifier.submissionpathfaculty_pubs/1050
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pagese17672


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