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Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation I

ABSTRACT: Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation I

PROVIDER: PRJNA1040912 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26844100_1.fastq.gz	Fastqsanger.gz
	SRR26844100_2.fastq.gz	Fastqsanger.gz
	SRR26844101_1.fastq.gz	Fastqsanger.gz
	SRR26844101_2.fastq.gz	Fastqsanger.gz
	SRR26844081_1.fastq.gz	Fastqsanger.gz

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Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation

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Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation II

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Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation

Project description:This RNA-Seq analysis compares gene expression of the pho7∆ fission yeast (Schizosaccharomyces pombe) strain prior to phosphate starvation (0 HR), i.e. in phosphate replete conditions, and at various times after phosphate starvation (4, 8, 12, 24, 36, and 48 HR) contrasting to the WT fission yeast S. pombe cells grown in phosphate replete conditions (WT 0HR)

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Factors governing the transcriptome changes and chronological lifespan of fission yeast during phosphate starvation II

Project description:This RNA-Seq analysis compares gene expression of the wild-type fission yeast (Schizosaccharomyces pombe) strain at various times after transfer to defined phosphate-replete ePMGT(+PO4) medium (2, 4, 8 HR) contrasting to the WT fission yeast S. pombe cells grown in phosphate-replete YES medium (0HR).

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TORC1 signaling pathway inhibition by rapamycin and caffeine affect lifespan, global gene expression and cell proliferation of fission yeast

Project description:Target of rapamycin complex 1 (TORC1) is implicated in growth control and aging from yeast to humans. Fission yeast is emerging as a popular model organism to study TOR signaling, although rapamycin has been thought to not affect cell growth in this organism. Here we analyzed the effects of rapamycin and caffeine, singly and combined, on multiple cellular processes in fission yeast. The two drugs led to diverse and specific phenotypes that depended on TORC1 signaling pathway inhibition, including prolonged chronological lifespan, inhibition of global translation, inhibition of cell growth and division, and reprogramming of global gene expression mimicking nitrogen starvation. Rapamycin and caffeine differentially affected these various TORC1-dependent processes. Combined drug treatment augmented most phenotypes and effectively blocked cell growth. Although rapamycin showed a much more subtle effect on global translation than did caffeine, rapamycin was more effective in prolonging chronological lifespan. Rapamycin prolonged the lifespan of non-growing cells only when applied during the growth phase but not when applied after cells had stopped proliferation. The doses of rapamycin and caffeine strongly correlated with growth inhibition and with lifespan extension. This comprehensive analysis will inform future studies into TORC1 function and cellular aging in fission yeast and beyond.

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Structural clusters of histone H3 and H4 residues regulate chronological lifespan in Saccharomyces cerevisiae [Other]

Project description:We have performed a comprehensive analysis of the involvement of histone H3 and H4 residues in the regulation of chronological lifespan in yeast. Residues where substitution resulted in the most pronounced lifespan extension are all on the exposed face of the nucleosome, with the exception of H3E50, which is present on the lateral surface, between two DNA gyres. Other residues that had a more modest effect on lifespan extension were concentrated at the extremities of the H3-H4 dimer, suggesting a role in stabilizing the dimer in its nucleosome frame. Residues implicated in a reduced lifespan were buried in the histone handshake motif, suggesting that these mutations destabilize the octamer structure. All residues exposed on the disk and that caused lifespan extension are known to interact with Sir3. We find that substitution of H4K16 and H4H18 cause Sir3 to redistribute from telomeres and silent mating loci to secondary positions, often enriched for Rap1 or Abf1 binding sites, whereas H3E50 does not. The redistributed Sir3 cause transcriptional repression at most of the new loci, including of genes where null mutants were previously shown to extend chronological lifespan. The transcriptomic profiles of H4K16 and H4H18 mutant strains are very similar, and compatible with a DNA replication stress response. This is distinct from the transcriptomic profile of H3E50, which matches strong induction of oxidative phosphorylation. We propose that different clusters of H3 and H4 residues are involved in either binding to non-histone proteins, or in destabilizing the association of the nucleosome DNA, or disrupting binding of a H3-H4 dimer in the nucleosome, or disturbing the structural stability of the octamer, each category impacting on chronological lifespan through a different path.

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