NDLI: Snf1 Kinase Connects Nutritional Pathways Controlling Meiosis in Saccharomyces cerevisiae

Content Provider	PubMed Central
Author	Honigberg, Saul M. Lee, Rita H.
Copyright Year	1998
Abstract	Glucose inhibits meiosis in Saccharomyces cerevisiae at three different steps (IME1 transcription, IME2 transcription, and entry into late stages of meiosis). Because many of the regulatory effects of glucose in yeast are mediated through the inhibition of Snf1 kinase, a component of the glucose repression pathway, we determined the role of SNF1 in regulating meiosis. Deleting SNF1 repressed meiosis at the same three steps that were inhibited by glucose, suggesting that glucose blocks meiosis by inhibiting Snf1. For example, the snf1Δ mutant completely failed to induce IME1 transcripts in sporulation medium. Furthermore, even when this block was bypassed by expression of IME1 from a multicopy plasmid, IME2 transcription and meiotic initiation occurred at only 10 to 20% of the levels seen in wild-type cells. The addition of glucose did not further inhibit IME2 transcription, suggesting that Snf1 is the primary mediator of glucose controls on IME2 expression. Finally, in snf1Δ cells in which both blocks on meiotic initiation were bypassed, early stages of meiosis (DNA replication and commitment to recombination) occurred, but later stages (chromosome segregation and spore formation) did not, suggesting that Snf1 controls later stages of meiosis independently from the two controls on meiotic initiation. Because Snf1 is known to activate the expression of genes required for acetate metabolism, it may also serve to connect glucose and acetate controls on meiotic differentiation.
Starting Page	4548
File Format	PDF
ISSN	10985549
e-ISSN	10985549
Journal	Molecular and Cellular Biology
Issue Number	8
Volume Number	18
Language	English
Publisher	American Society for Microbiology
Publisher Date	1998-08-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology

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