Inactivation of Ku-mediated end joining suppresses mec1Delta lethality by depleting the ribonucleotide reductase inhibitor Sml1 through a pathway controlled by Tel1 kinase and the Mre11 complex.

@article{Corda2005InactivationOK,
  title={Inactivation of Ku-mediated end joining suppresses mec1Delta lethality by depleting the ribonucleotide reductase inhibitor Sml1 through a pathway controlled by Tel1 kinase and the Mre11 complex.},
  author={Yves Corda and Sang Eun Lee and Sylvine Guillot and Andr{\'e} Walther and Julie Sollier and Ayelet Arbel-Eden and James E Haber and Vincent G{\'e}li},
  journal={Molecular and cellular biology},
  year={2005},
  volume={25 23},
  pages={10652-64}
}
RAD53 and MEC1 are essential Saccharomyces cerevisiae genes required for the DNA replication and DNA damage checkpoint responses. Their lethality can be suppressed by increasing the intracellular pool of deoxynucleotide triphosphates. We report that deletion of YKU70 or YKU80 suppresses mec1Delta, but not rad53Delta, lethality. We show that suppression of mec1Delta lethality is not due to Ku--associated telomeric defects but rather results from the inability of Ku- cells to efficiently repair… CONTINUE READING

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