Crossing-over is an essential aspect of meiosis that is required for accurate chromosome segregation and the formation of new allele combinations. Crossovers form by the process of homologous recombination in which a broken chromosome utilizes an intact homologous chromosome as a template for repair. Meiotic recombination is initiated by programmed DNA double-strand breaks (DSBs). The ends of these breaks interact sequentially with a homologous chromosome to form two distinct joint molecule intermediates, the single-end invasion (SEI), and the double Holliday junction (dHJ). Nucleolytic cleavage of the dHJ subsequently yields crossover products. I am studying the molecular mechanism of joint molecule formation during meiosis in budding yeast using molecular assays to monitor the DNA events of recombination in vivo. My thesis project aims to determine why meiotic cells express a dedicated strand-exchange protein, Dmc1, as well as the mitotic strand-exchange protein, Rad51.
MCB NIH Training Grant (2007-2009).
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Publications
Oh SD, Lao JP, Hwang PY, Taylor AF, Smith GR, Hunter N. "BLM ortholog, Sgs1, prevents aberrant crossing-over by suppressing formation of multichromatid joint molecules," Cell. 2007 Jul 27;130(2):259-72.
Lao JP, Oh SD, Shinohara M, Shinohara A, Hunter N. "Rad52 promotes postinvasion steps of meiotic double-strand-break repair," Mol Cell. 2008 Feb 29;29(4):517-24.
Oh SD, Lao JP, Taylor AF, Smith GR and Hunter N (2008). RecQ Helicase, Sgs1, and XPF-Family Endonuclease, Mus81-Mms4, Resolve Aberrant Joint Molecules During Meiotic Recombination. Molecular Cell in press.
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