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Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

ABSTRACT: This RNA-Seq analysis compares gene expression of fission yeast (Schizosaccharomyces pombe) strains prior to phosphate starvation (0 HR) 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)

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE213459 | GEO | 2023/01/19

REPOSITORIES: GEO

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

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Project description:Inorganic phosphate is an essential nutrient acquired by cells from their environment. Here we characterize the adaptative responses of fission yeast to chronic phosphate starvation, during which cells enter a state of quiescence, initially fully reversible upon replenishing phosphate after 2 days but resulting in gradual loss of viability during 4 weeks of starvation. Time-resolved analyses of changes in mRNA levels revealed a coherent transcriptional program in which phosphate dynamics and autophagy were upregulated, while the machineries for rRNA synthesis and ribosome assembly, and for tRNA synthesis and maturation, were downregulated in tandem with global repression of genes encoding ribosomal proteins and translation factors. Consistent with the transcriptome changes, proteome analysis highlighted global depletion of 102 ribosomal proteins. Concomitant with this ribosomal protein deficit, 28S and 18S rRNAs became vulnerable to site-specific cleavages that generated temporally stable rRNA fragments. The finding that Maf1, a repressor of RNA polymerase III transcription, was upregulated during phosphate starvation prompted a hypothesis that its activity might prolong lifespan of the quiescent cells by limiting production of tRNAs. Indeed, we found that deletion of maf1 results in precocious death of phosphate-starved cells via a distinctive starvation-induced pathway associated with tRNA overproduction and dysfunctional tRNA biogenesis.

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