PMC:4502372 / 37603-38418 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":"The finding that the delay in colony formation in sea3Δ mutants after DNA damage was not caused by defects in the ability or kinetics of repair nor prolonged activation of the DNA damage checkpoint (Figure 3) was surprising because no studies have shown a growth defect post-DNA repair without accompanying Rad53 hyperphosphorylation. Instead, we found the delay was dependent on tryptophan auxotrophy (Figure 5A), uncovering the importance of tryptophan after DNA damage. Consistent with this finding, Tat2 protein levels increased in both wild-type and the sea3Δ mutant postbreak induction when Rad53 hyperphosphorylation was high but declined more slowly, suggesting that, even as the DNA damage checkpoint was alleviated, the demand for tryptophan import remained elevated (Figure 3C, Figure 5C, and Figure S9).","tracks":[]}