Ssd1 and the cell wall integrity pathway promote entry, maintenance, and recovery from quiescence in budding yeast.

Wild Saccharomyces cerevisiae strains are typically diploid. When faced with glucose and nitrogen limitation they can undergo meiosis and sporulate. Diploids can also enter a protective, nondividing cellular state or quiescence. The ability to enter quiescence is highly reproducible but shows broad natural variation. Some wild diploids can only enter cellular quiescence, which indicates that there are conditions in which sporulation is lost or selected against. Others only sporulate, but if sporulation is disabled by heterozygosity at the IME1 locus, those diploids can enter quiescence. W303 haploids can enter quiescence, but their diploid counterparts cannot. This is the result of diploidy, not mating type regulation. Introduction of SSD1 to W303 diploids switches fate, in that it rescues cellular quiescence and disrupts the ability to sporulate. Ssd1 and another RNA-binding protein, Mpt5 (Puf5), have parallel roles in quiescence in haploids. The ability of these mutants to enter quiescence, and their long-term survival in the quiescent state, can be rescued by exogenously added trehalose. The cell wall integrity pathway also promotes entry, maintenance, and recovery from quiescence through the Rlm1 transcription factor.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}