Homologous recombination is an important pathway for the repair of DNA damage by radiation, chemicals, and endogenous cellular processes. However, recombination must be carefully controlled as deleterious genome rearrangements can result from unrestricted recombination between numerous, dispersed repetitive sequences. Since the majority of these repeats are 300 bp or shorter in eukaryotes, the control of recombination between these short sequences is more stringent than for longer sequences. Several of the genes known to mediate the response to radiation in the budding yeast S. cerevisiae also control short-sequence recombination (SSR). The goal of the proposed research program is to further investigate important interactions between several of the most critical factors at the genetic and molecular levels. DNA fragment insertion assays in cells with mutant SSR factors will be used to explore the effect of specific defects, both alone and in combination, on SSR. Repair of a genomic double-strand break by recombination will be used to monitor the kinetics of SSR in these mutants. Ligation mediated PCR will be employed to track and quantitate secondary breaks created during SSR. Chromatin immunoprecipitation will be used to follow the interaction of several important protein complexes and the recombination substrates. This combination of genetic and physical methods will promote a more thorough understanding of several of the molecular interactions critical for SSR, and the maintenance of genome stability.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Research Project (R01)
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Radiation Study Section (RAD)
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Anderson, Richard A
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City of Hope/Beckman Research Institute
United States
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Sheldon, Kathryn E; Shandilya, Harish; Kepka-Lenhart, Diane et al. (2013) Shaping the murine macrophage phenotype: IL-4 and cyclic AMP synergistically activate the arginase I promoter. J Immunol 191:2290-8
Pannunzio, Nicholas R; Manthey, Glenn M; Bailis, Adam M (2010) RAD59 and RAD1 cooperate in translocation formation by single-strand annealing in Saccharomyces cerevisiae. Curr Genet 56:87-100
Manthey, Glenn M; Bailis, Adam M (2010) Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae. PLoS One 5:e11889
Manthey, Glenn M; Naik, Nilan; Bailis, Adam M (2009) Msh2 blocks an alternative mechanism for non-homologous tail removal during single-strand annealing in Saccharomyces cerevisiae. PLoS One 4:e7488
Meyer, Damon H; Bailis, Adam M (2008) Telomerase deficiency affects the formation of chromosomal translocations by homologous recombination in Saccharomyces cerevisiae. PLoS One 3:e3318
Meyer, Damon H; Bailis, Adam M (2008) Mating type influences chromosome loss and replicative senescence in telomerase-deficient budding yeast by Dnl4-dependent telomere fusion. Mol Microbiol 69:1246-54
Pannunzio, Nicholas R; Manthey, Glenn M; Bailis, Adam M (2008) RAD59 is required for efficient repair of simultaneous double-strand breaks resulting in translocations in Saccharomyces cerevisiae. DNA Repair (Amst) 7:788-800
Meyer, Damon H; Bailis, Adam M (2007) Telomere dysfunction drives increased mutation by error-prone polymerases Rev1 and zeta in Saccharomyces cerevisiae. Genetics 175:1533-7
Manthey, Glenn M; Bailis, Adam M (2002) Multiple pathways promote short-sequence recombination in Saccharomyces cerevisiae. Mol Cell Biol 22:5347-56