A Syntenic Cross Species Aneuploidy Genetic Screen Links RCAN1 Expression to β-Cell Mitochondrial Dysfunction in Type 2 Diabetes
Publication Date
May 19, 2016
Journal
PLOS Genetics
Authors
Heshan Peiris, Michael D. Duffield, Joao Fadista, Claire F. Jessup, et al
Volume
12
Issue
5
Pages
e1006033
DOI
https://dx.plos.org/10.1371/journal.pgen.1006033
Publisher URL
http://journals.plos.org/plosgenetics/article?id=10.1371%2Fjournal.pgen.1006033
Web of Science
000377197100034
Scopus
84974602795
Mendeley
http://www.mendeley.com/research/syntenic-cross-species-aneuploidy-genetic-screen-links-rcan1-expression-%CE%B2cell-mitochondrial-dysfunct
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Mendeley | Further Information

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Ross", "last_name"=>"Laybutt", "scopus_author_id"=>"6603447404"}, {"first_name"=>"P. Toby", "last_name"=>"Coates", "scopus_author_id"=>"35598001200"}, {"first_name"=>"Sijun", "last_name"=>"Yang", "scopus_author_id"=>"56888029400"}, {"first_name"=>"Charlotte", "last_name"=>"Ling", "scopus_author_id"=>"8300751400"}, {"first_name"=>"Leif", "last_name"=>"Groop", "scopus_author_id"=>"21634758500"}, {"first_name"=>"Melanie A.", "last_name"=>"Pritchard", "scopus_author_id"=>"7102684132"}, {"first_name"=>"Damien J.", "last_name"=>"Keating", "scopus_author_id"=>"8706090000"}], "year"=>2016, "source"=>"PLoS Genetics", "identifiers"=>{"scopus"=>"2-s2.0-84974602795", "pui"=>"610810160", "sgr"=>"84974602795", "isbn"=>"1553-7404 (Electronic)\r1553-7390 (Linking)", "issn"=>"15537404", "pmid"=>"27195491", "doi"=>"10.1371/journal.pgen.1006033"}, "id"=>"434e13a4-3b5b-3c08-85b8-e22f27777dc8", "abstract"=>"Type 2 diabetes (T2D) is a complexmetabolic disease associated with obesity, insulin resistance and hypoinsulinemia due to pancreatic β-cell dysfunction. Reduced mitochon- drial function is thought to be central to β-cell dysfunction. Mitochondrial dysfunction and reduced insulin secretion are also observed in β-cells of humans with the most common human genetic disorder, Down syndrome (DS, Trisomy 21). To identify regions of chromo- some 21 that may be associated with perturbed glucose homeostasis we profiled the gly- caemic status of different DS mousemodels. The Ts65Dn and Dp16 DSmouse lines were hyperglycemic, while Tc1 and Ts1Rhr mice were not, providing us with a region of chromo- some 21 containing genes that cause hyperglycemia. Wethen examined whether any of these genes were upregulated in a set of ~5,000 gene expression changes we had identi- fied in a large gene expression analysis of human T2D β-cells. This approach produced a single gene, RCAN1, as a candidate gene linking hyperglycemia and functional changes in T2D β-cells. Further investigations demonstrated that RCAN1methylation is reduced in human T2D islets at multiple sites, correlating with increased expression. RCAN1 protein expression was also increased in db/dbmouse islets and in human and mouse islets exposed to high glucose. Mice overexpressing RCAN1 had reduced in vivo glucose-stimu- lated insulin secretion and their β-cells displayed mitochondrial dysfunction including hyper- polarisedmembrane potential, reduced oxidative phosphorylation and low ATP production. This lack of β-cell ATP had functional consequences by negatively affecting both glucose- stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Thus, from amongst the myriad of gene expression changes occurring in T2D β-cells where we had little knowledge of which changes cause β-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to β-cell mitochondrial dysfunction in T2D.", "link"=>"http://www.mendeley.com/research/syntenic-cross-species-aneuploidy-genetic-screen-links-rcan1-expression-%CE%B2cell-mitochondrial-dysfunct", "reader_count"=>27, "reader_count_by_academic_status"=>{"Unspecified"=>3, "Professor > Associate Professor"=>2, "Student > Doctoral Student"=>2, "Researcher"=>1, "Student > Ph. D. Student"=>5, "Student > Postgraduate"=>1, "Other"=>1, "Student > Master"=>4, "Student > Bachelor"=>5, "Professor"=>3}, "reader_count_by_user_role"=>{"Unspecified"=>3, "Professor > Associate Professor"=>2, "Student > Doctoral Student"=>2, "Researcher"=>1, "Student > Ph. D. 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