Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination

  • Alvaro D
  • Lisby M
  • Rothstein R
N/ACitations
Citations of this article
5Readers
Mendeley users who have this article in their library.

Abstract

To investigate the DNA damage response, we undertook a genome-wide study in Saccharomyces cerevisiae and identified 86 gene deletions that lead to increased levels of spontaneous Rad52 foci in proliferating diploid cells. More than half of the genes are conserved across species ranging from yeast to humans. Along with genes involved in DNA replication, repair, and chromatin remodeling, we found 22 previously uncharacterized open reading frames. Analysis of recombination rates and synthetic genetic interactions with rad52D suggests that multiple mechanisms are responsible for elevated levels of spontaneous Rad52 foci, including increased production of recombinogenic lesions, sister chromatid recombination defects, and improper focus assembly/disassembly. Our cell biological approach demonstrates the diversity of processes that converge on homologous recombination, protect against spontaneous DNA damage, and facilitate efficient repair. Citation: Alvaro D, Lisby M, Rothstein R (2007) Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. PLoS Genet 3(12): e228.

Cite

CITATION STYLE

APA

Alvaro, D. A., Lisby, M., & Rothstein, R. (2005). Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. PLoS Genetics, preprint(2007), e228. https://doi.org/10.1371/journal.pgen.0030228.eor

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free