Title

Genetic and molecular characterization of nutritional signaling pathways regulating meiosis in Saccharomyces cerevisiae

Date of Award

5-2002

Degree Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Biology

Advisor(s)

Saul Honigberg

Keywords

Nutritional, Meiosis, Glucose

Subject Categories

Molecular Genetics

Abstract

Environmental signals regulate many cell differentiation processes in eukaryotes. In the yeast Saccharomyces cerevisiae , environmental signals regulate meiosis. Initiation of meiosis requires the expression of IME1 , an essential gene for meiosis. Expression of the IME1 is blocked by glucose. Previous work suggested that in low concentrations of glucose, overexpression of IME1 was sufficient to induce high levels of recombination. My work demonstrates that these cells undergo the early meiotic events including DNA replication, commitment to recombination, and synaptonemal complex formation and dissolution. In contrast, the late meiotic events including chromosome segregation, commitment to meiosis, and spore formation do not occur. These cells are stably arrested and when transferred to sporulation medium, are able to complete meiosis. This implies that extracellular nutrients regulate meiosis in yeast at both early and late stages of meiosis.

Specifically, glucose was shown to regulate meiosis at multiple stages ( IME1 transcription, IME2 transcription, and entry into late stages of meiosis). Therefore, since many cellular responses to glucose in yeast are mediated through the glucose repression pathway, the central component of this pathway was analyzed for its role in meiosis.

My work confirmed that SNF1 is required both prior to and after DNA replication. Given this finding, I constructed deletion mutants of other components of the glucose repression pathway ( SNF3, RGT2, RGT1, CAT8 , and SIP4 ) to determine their role in glucose repression of meiosis. My results suggest that SNF3 and RGT2 are involved, in part, in glucose repression of meiosis. Furthermore, while the downstream component RGT1 is not involved in glucose repression, cells lacking RGT1 were mildly defective in meiosis. Candidates for Snf1 targets were also tested. Deletion of the transcriptional repressors MG1 and YHP1 fails to suppress the meiotic defects of a snflΔ mutant. Deletion of CAT8 , but not SIP4 , caused severe defects in meiosis. Therefore, this works demonstrates that only a subset of the glucose repression pathway components are involved in regulation of meiosis.

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