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Gcn5- and Bre1-mediated Set2 degradation promotes chronological aging of Saccharomyces cerevisiae

ABSTRACT: Gcn5- and Bre1-mediated Set2 degradation promotes chronological aging of Saccharomyces cerevisiae

PROVIDER: PRJNA912604 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22746561_1.fastq.gz	Fastqsanger.gz
	SRR22746561_2.fastq.gz	Fastqsanger.gz
	SRR22746562_1.fastq.gz	Fastqsanger.gz
	SRR22746562_2.fastq.gz	Fastqsanger.gz
	SRR22746563_1.fastq.gz	Fastqsanger.gz

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Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [RNA-seq]

Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.

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Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [ChIP-seq]

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Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [ChIP-seq]

Project description:Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [ChIP-seq]

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Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [RNA-seq]

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Gcn5- and Bre1-mediated Set2 degradation promotes chronological aging of Saccharomyces cerevisiae

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

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Histone H4 acetylation in wild-type, ASF1, SET2 and ASF1 SET2 deletion yeast strains

Project description:ChIP-on chip assays to measure the change in histone acetylation over the yeast genome, in ASF1, SET2 and ASF1 SET2 deletion yeast strains compared to the wild-type control. ChIPs of AcH4 from wild-type, ASF1, SET2 and ASF1 SET2 deletion yeast strains were normalized to the H3 enrichment.

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Project description:Skeletal muscle is a post-mitotic tissue that exhibits an extremely low turnover in the absence of disease or injury. At the same time, muscle possesses remarkable regenerative capacity mediated by satellite cells (SCs) that reside in close association with individual myofibers, underneath the fiber’s basal lamina. Consistent with the low turnover of the muscle, SCs in adult animals are mitotically quiescent and therefore provide an excellent model to study stem cell quiescence. As an organism grows older, the resident stem cells are exposed to a deteriorating environment and experience chronological aging. In stem cells with high turnover, the effects of chronological aging are superimposed upon the effects of the replicative aging that results from DNA replication and cell division. On the contrary, SCs experience minimal replicative aging due to their low turnover. They are thus a good model to study the consequence of chronological aging of quiescent stem cells. We performed microarray analysis of quiescent and activated SCs from both young and aged mice to understand the global gene expression profile underlying stem cell properties such as quiecence and self-renewal, and to understand how the transcriptome of a quiescent stem cell pouplation changes with age.

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Project description:H3K36 methylation by Set2 targets Rpd3S histone deacetylase to 3Ã¢ÂÂ transcribed regions, repressing internal cryptic promoters and slowing elongation. To further explore the function of this pathway, global transcription was analyzed in yeast experiencing a series of carbon source shifts. Many previously unreported cryptic ncRNAs are induced by specific carbon sources, showing that cryptic promoters can be environmentally regulated. Also, approximately 230 mRNA genes show altered induction or repression upon SET2 deletion. A majority of Set2-repressed genes have overlapping lncRNA transcription. At these promoters, H3K36me3 and deacetylation by Rpd3S leads to slower or reduced induction. Unexpectedly, Set2 derepresses 159 genes, apparently by mediating a balance between Rpd3S and Rpd3L. Therefore, in addition to repression of cryptic transcription, H3K36 methylation maintains optimal expression dynamics of many mRNAs.

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