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H3K36 methylation promotes longevity by enhancing transcriptional fidelity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans Saccharomyces cerevisiae

PROVIDER: GSE65767 | GEO | 2015/07/17

SECONDARY ACCESSION(S): PRJNA274973

REPOSITORIES: GEO

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H3K36 methylation promotes longevity by enhancing transcriptional fidelity.

Project description:Epigenetic mechanisms, including histone post-translational modifications, control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging phenomenon of shortened life span, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a life span screen in Saccharomyces cerevisiae that is designed to identify amino acid residues of histones that regulate yeast replicative aging. Our results reveal that lack of sustained histone H3K36 methylation is commensurate with increased cryptic transcription in a subset of genes in old cells and with shorter life span. In contrast, deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes, suppresses cryptic transcript initiation, and extends life span. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to loss of transcriptional precision that is detrimental to life span, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.

| S-EPMC4511212 | biostudies-literature

H3K36 methylation promotes longevity by enhancing transcriptional fidelity [ChIP-Seq]

Project description:Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.

2015-07-17 | GSE65766 | GEO

H3K36 methylation promotes longevity by enhancing transcriptional fidelity [Yeast RNA-Seq]

2015-07-17 | GSE65764 | GEO

H3K36 methylation promotes longevity by enhancing transcriptional fidelity [Worm RNA-Seq]

2015-07-17 | GSE65765 | GEO

H3K36 methylation promotes longevity by enhancing transcriptional fidelity

Project description:H3K36 methylation promotes longevity by enhancing transcriptional fidelity

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H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-13 | E-GEOD-69291 | biostudies-arrayexpress

H3K36 Methylation Regulates Nutrient Stress Response in Saccharomyces cerevisiae by Enforcing Transcriptional Fidelity.

Project description:Set2-mediated histone methylation at H3K36 regulates diverse activities, including DNA repair, mRNA splicing, and suppression of inappropriate (cryptic) transcription. Although failure of Set2 to suppress cryptic transcription has been linked to decreased lifespan, the extent to which cryptic transcription influences other cellular functions is poorly understood. Here, we uncover a role for H3K36 methylation in the regulation of the nutrient stress response pathway. We found that the transcriptional response to nutrient stress was dysregulated in SET2-deleted (set2?) cells and was correlated with genome-wide bi-directional cryptic transcription that originated from within gene bodies. Antisense transcripts arising from these cryptic events extended into the promoters of the genes from which they arose and were associated with decreased sense transcription under nutrient stress conditions. These results suggest that Set2-enforced transcriptional fidelity is critical to the proper regulation of inducible and highly regulated transcription programs.

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SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-10 | GSE127060 | GEO

Tet1 and hydroxymethylcytosine in transcription and DNA methylation fidelity

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2011-04-13 | E-GEOD-24843 | biostudies-arrayexpress

PRC2 coordinates lineage fidelity and DNA methylation during ESC differentiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-11-17 | E-GEOD-53508 | biostudies-arrayexpress