TOR and PKA pathways synergize at the level of the Ste11 transcription factor to prevent mating and meiosis in fission yeast.

BACKGROUND:In the fission yeast Schizosaccharomyces pombe, the TOR (target of rapamycin) and (protein kinase A) signaling transduction pathways regulate the expression of genes required for cell growth and sexual differentiation in response to the nutritional environment. Inhibition of Tor2 signaling results in the induction of genes involved in sexual differentiation, and the cells undergo mating and meiosis, even under good nutritional conditions. The same phenotype is observed in mutants in which the duanyu1529 pathway is inactive. By contrast, Tor2 overexpression or mutations that hyperactivate duanyu1529 signaling impair sexual differentiation, even under poor nutritional conditions. Accordingly, a very important question is to understand the molecular mechanism by which these two pathways coordinately regulate gene expression in response to nutrients. METHODOLOGY/PRINCIPAL FINDINGS:Here we demonstrate that TOR and duanyu1529 pathways operate coordinately to negatively regulate sexual differentiation by inhibiting the nuclear accumulation of the Ste11 transcription factor. However, the Tor2 pathway is unable to block the nuclear localization of Ste11 under good nutritional conditions when the duanyu1529 pathway is inactive. Using microarray analyses, we found that both pathways inhibit sexual differentiation by blocking ste11-dependent gene expression. CONCLUSIONS/SIGNIFICANCE:We conclude that both the duanyu1529 and the TOR pathways inhibit Ste11 nuclear accumulation to repress Ste11-dependent gene expression. However, the duanyu1529 pathway plays a quantitatively more important role than the TOR pathway in this process.

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