Abstract
Meiosis is the process by which diploid cells undergo DNA synthesis, homologous recombination and pairing, followed by the reductional division then the equational division. I present work in this PhD thesis which furthers the understanding of the coordination of the initiation of meiotic recombination and the reductional division. Ten genes are required to initiate recombination in Saccharomyces cerevisiae. The presence of a subset of recombination initiation proteins creates a Recombination Initiation Signal (RIS) that delays the start of MI in wild type cells. I present experiments demonstrating the first division kinetics of the two remaining recombination initiation genes that our lab had not yet studied. Rec107 is part of the RIS, while Ski8 is not. The RIS is conserved in a divergent Saccharomyces strain background. rec102 and rec104 SK1 strains both start the first division earlier that wild type SK1 strains. I present evidence that suggests that the RIS acts independently of the pathway that controls securin (PDS1) degradation. The work in this thesis expands our knowledge of the mechanism by which the RIS delays the reductional division. In this thesis I present experiments showing that the DNA damage, spindle and S phase checkpoints do not transduce the RIS. I establish the meiosis-specific candidate Mek1 as a candidate for relaying the RIS. Lastly, experiments described in these chapters show that the transcriptional activator of Middle Meiosis, NDT80, is the target of the RIS. NDT80 transcription and activity are both necessary and sufficient to affect an earlier reductional division, similar to the early MI seen in RIS mutants.
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