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{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/4502372","sourcedb":"PMC","sourceid":"4502372","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4502372","text":"To determine whether Sea3 and, perhaps, TORC1 signaling were required for growth in response to other stress conditions, we plated sea3∆ mutants in both the YPH274 and BIR assay strain backgrounds on YPD containing a low concentration of glucose (0.25% compared to 2% in standard YPD), high salt (0.5 M NaCl added to standard YPD), or hydrogen peroxide (3 mM H2O2 added to standard YPD), and at high temperature (37°). We found the sea3Δ mutant in the YPH274 strain background had a growth delay on medium containing high salt, an effect that was mediated through TORC1 signaling as it was rescued by deletion of IML1 (Figure S5A). However, a growth delay was not observed on high salt with the sea3∆ mutant in the BIR assay strain background (Figure S5B), suggesting the phenotype was influenced by strain specific factors and not solely the absence of Sea3. In both strain backgrounds, we found that Sea3 was not required for growth in response to any of the other stresses tested (Figure S5). Taken together, although there are some strain specific differences, sea3Δ mutants experience a growth defect under conditions that induce DSBs and under conditions of high salt in a TORC1-dependent manner.","tracks":[]}