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10.1186/s13059-017-1185-3 http://scihub22266oqcxt.onion/10.1186/s13059-017-1185-3 C5370462!5370462!28351383     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28351383&cmd=llinks): Failed to open stream: HTTP request failed! 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Diverse interventions that extend mouse lifespan suppress shared age-associated epigenetic changes at critical gene regulatory regions |pdf=|usr=}}{{28351383}} gab.com Text Diverse interventions that extend mouse lifespan suppress shared age-associated epigenetic changes at critical gene regulatory regions JO: Genome Biol http://www.kidney.de/pget.php?&tw=1&pmid=28351383 #FOAvip Background: Age-associated epigenetic changes are implicated in aging. Notably, age-associated DNA methylation changes comprise a so-called aging ?clock?, a robust biomarker of aging. However, while genetic, dietary and drug interventions can extend lifespan, their impact on the epigenome is uncharacterised. To fill this knowledge gap, we defined age-associated DNA methylation changes at the whole-genome, single-nucleotide level in mouse liver and tested the impact of longevity-promoting interventions, specifically the Ames dwarf Prop1df/df mutation, calorie restriction and rapamycin. Results: In wild-type mice fed an unsupplemented ad libitum diet, age-associated hypomethylation was enriched at super-enhancers in highly expressed genes critical for liver function. Genes harbouring hypomethylated enhancers were enriched for genes that change expression with age. Hypermethylation was enriched at CpG islands marked with bivalent activating and repressing histone modifications and resembled hypermethylation in liver cancer. Age-associated methylation changes are suppressed in Ames dwarf and calorie restricted mice and more selectively and less specifically in rapamycin treated mice. Conclusions: Age-associated hypo- and hypermethylation events occur at distinct regulatory features of the genome. Distinct longevity-promoting interventions, specifically genetic, dietary and drug interventions, suppress some age-associated methylation changes, consistent with the idea that these interventions exert their beneficial effects, in part, by modulation of the epigenome. This study is a foundation to understand the epigenetic contribution to healthy aging and longevity and the molecular basis of the DNA methylation clock. Electronic supplementary material: The online version of this article (doi:10.1186/s13059-017-1185-3) contains supplementary material, which is available to authorized users. Twit Text FOAVip Diverse interventions that extend mouse lifespan suppress shared age-associated epigenetic changes at critical gene regulatory regions ????Genome Biol http://www.kidney.de/pget.php?&tw=1&pmid=28351383 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28351383 #FOAvip English Wikipedia <ref>{{Cite pmid|28351383}}</ref> Diverse interventions that extend mouse lifespan suppress shared age-associated epigenetic changes at critical gene regulatory regions #MMPMID28351383 Cole JJ; Robertson NA; Rather MI; Thomson JP; McBryan T; Sproul D; Wang T; Brock C; Clark W; Ideker T; Meehan RR; Miller RA; Brown-Borg HM; Adams PD Genome Biol 2017[]; 18 (ä): ä PMID28351383show ga Background: Age-associated epigenetic changes are implicated in aging. Notably, age-associated DNA methylation changes comprise a so-called aging ?clock?, a robust biomarker of aging. However, while genetic, dietary and drug interventions can extend lifespan, their impact on the epigenome is uncharacterised. To fill this knowledge gap, we defined age-associated DNA methylation changes at the whole-genome, single-nucleotide level in mouse liver and tested the impact of longevity-promoting interventions, specifically the Ames dwarf Prop1df/df mutation, calorie restriction and rapamycin. Results: In wild-type mice fed an unsupplemented ad libitum diet, age-associated hypomethylation was enriched at super-enhancers in highly expressed genes critical for liver function. Genes harbouring hypomethylated enhancers were enriched for genes that change expression with age. Hypermethylation was enriched at CpG islands marked with bivalent activating and repressing histone modifications and resembled hypermethylation in liver cancer. Age-associated methylation changes are suppressed in Ames dwarf and calorie restricted mice and more selectively and less specifically in rapamycin treated mice. Conclusions: Age-associated hypo- and hypermethylation events occur at distinct regulatory features of the genome. Distinct longevity-promoting interventions, specifically genetic, dietary and drug interventions, suppress some age-associated methylation changes, consistent with the idea that these interventions exert their beneficial effects, in part, by modulation of the epigenome. This study is a foundation to understand the epigenetic contribution to healthy aging and longevity and the molecular basis of the DNA methylation clock. Electronic supplementary material: The online version of this article (doi:10.1186/s13059-017-1185-3) contains supplementary material, which is available to authorized users. äDiverse interventions that extend mouse lifespan suppress shared age-a(epmc).pdf DeepDyve Pubget Overpricing