PMC:4502372 / 8435-9283 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/4502372","sourcedb":"PMC","sourceid":"4502372","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4502372","text":"TORC1 also contributes to the DNA damage response (DDR) secondary to DSBs. Treatment of cells with rapamycin, which directly inhibits the TORC1 complex, and then with the DNA-damaging agent methyl methanesulfonate results in suppression of the Rad53-dependent up-regulation of ribonucleotide reductase (RNR) genes, RNR1 and RNR3, and decreased survival (Shen et al. 2007). In addition, strains bearing RNR gene deletions have decreased survival when treated with both rapamycin and methyl methanesulfonate, leading to the hypothesis that survival of cells incurring DNA damage requires TORC1 enforcement of nucleotide pools sufficient for DNA synthesis postdamage. Interestingly, Sea3 has been found in genome-wide screens to physically interact with Yku80, Srs2, and Rfa3, all of which are DNA repair proteins (Ho et al. 2002; Chiolo et al. 2005).","tracks":[]}