PMC:4502372 / 21317-22415 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":"To determine whether the growth delay was caused by a general sensitivity to galactose (rather than the DSB induced by galactose), we took sea3Δ mutants in the BIR strain background that had been plated previously on galactose, had undergone BIR repair of the DSB and, therefore, would not sustain another HO-induced DSB when replated on galactose, and compared their growth on galactose to sea3Δ mutants that had not been previously exposed to galactose and, therefore, would undergo DSB induction when plated on galactose. If the growth delay of the sea3Δ mutants on galactose were simply due to a general sensitivity to galactose, then the presence or absence of a cleavable HO cut site would not matter and both types of sea3Δ mutants would be equally sensitive to galactose. We found, however, that when the sea3Δ mutants that were originally plated on galactose were re-plated on galactose, quantifiable colonies appeared sooner (Figure S2; see also Figure 5A and Figure S8A), suggesting that the delay in colony formation in the sea3Δ mutant was not simply due to a sensitivity to galactose.","tracks":[]}