Type
Text
Type
Thesis
Advisor
Hollingsworth, Nancy | Neiman, Aaron.
Date
2016-12-01
Keywords
Biochemistry -- Genetics
Department
Department of Biochemistry and Cell Biology
Language
en_US
Source
This work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.
Identifier
http://hdl.handle.net/11401/76896
Publisher
The Graduate School, Stony Brook University: Stony Brook, NY.
Format
application/pdf
Abstract
Meiosis is a specialized type of cell division, which produces haploid daughter cells from diploid parental cells. Meiotic recombination is initiated by the introduction of programmed DNA double strand breaks (DSBs), which are catalyzed by an evolutionarily conserved, meiosis-specific endonuclease, Spo11. Meiotic cells monitor the repair of Spo11-induced DSBs via the meiotic recombination checkpoint (MRC), which is activated in response to DSBs made during meiotic prophase. The MRC ensures proper repair of DSBs prior to entry into the first meiotic division. The Mec1 checkpoint kinase is recruited to resected DSBs via the 9-1-1 complex containing Rad17, Mec3 and Ddc1. Mec1 phosphorylation of Hop1 allows recruitment of the meiosis-specific kinase Mek1 to chromosomes where Mek1 is activated. Mek1 phosphorylation of substrates then ensures that DSBs are repaired in a Dmc1-dependent manner. My thesis focused on identifying the consequences of a putative Mek1 phosphorylation site on Rad17 in an attempt to further understand the function of Mek1 in meiosis in the budding yeast, Saccharomyces cerevisiae. | 44 pages
Recommended Citation
Rahat, Madeeha, "Functional consequences of a putative Mek1 phosphorylation site on Rad17 during meiosis in Saccharomyces cerevisiae" (2016). Stony Brook Theses and Dissertations Collection, 2006-2020 (closed to submissions). 2770.
https://commons.library.stonybrook.edu/stony-brook-theses-and-dissertations-collection/2770