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The DNA damage checkpoint pathway promotes extensive resection and nucleotide synthesis to facilitate homologous recombination repair and genome stability in fission yeast by Elizabeth J. Blaikley; Helen Tinline-Purvis; Torben R. Kasparek; Samuel Marguerat; Sovan Sarkar; Lydia Hulme; Sharon Hussey; Boon-Yu Wee; Rachel S. Deegan; Carol A. Walker; Chen-Chun Pai; Jürg Bähler; Takuro Nakagawa; Timothy C. Humphrey is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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DNA double-strand breaks (DSBs) can cause chromosomal rearrangements and extensive loss of heterozygosity (LOH), hallmarks of cancer cells. Yet, how such events are normally suppressed is unclear. Here we identify roles for the DNA damage checkpoint pathway in facilitating homologous recombination (HR) repair and suppressing extensive LOH and chromosomal rearrangements in response to a DSB. Accordingly, deletion of Rad3^ATR^, Rad26^ATRIP^, Crb2^53BP1^ or Cdc25 overexpression leads to reduced HR and increased break-induced chromosome loss and rearrangements. We find the DNA damage checkpoint pathway facilitates HR, in part, by promoting break-induced Cdt2-dependent nucleotide synthesis. We also identify additional roles for Rad17, the 9-1-1 complex and Chk1 activation in facilitating break-induced extensive resection and chromosome loss, thereby suppressing extensive LOH. Loss of Rad17 or the 9-1-1 complex results in a striking increase in break-induced isochromosome formation and very low levels of chromosome loss, suggesting the 9-1-1 complex acts as a nuclease processivity factor to facilitate extensive resection. Further, our data suggest redundant roles for Rad3^ATR^ and Exo1 i

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Author

Elizabeth J. Blaikley; Helen Tinline-Purvis; Torben R. Kasparek; Samuel Marguerat; Sovan Sarkar; Lydia Hulme; Sharon Hussey; Boon-Yu Wee; Rachel S. Deegan; Carol A. Walker; Chen-Chun Pai; Jürg Bähler; Takuro Nakagawa; Timothy C. Humphrey

Publisher

Oxford University Press (OUP)

Published

2014

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)