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• W2019902203 abstract "ABSTRACT Recombinational repair-dependent mutants identify ways to avoid chromosomal lesions. Starting with a recBC (Ts) strain of Escherichia coli , we looked for mutants unable to grow at 42°C in conditions that inactivate the RecBCD(Ts) enzyme. We isolated insertions in ackA and pta , which comprise a two-gene operon responsible for the acetate↔acetyl coenzyme A interconversion. Using precise deletions of either ackA or pta , we showed that either mutation makes E. coli cells dependent on RecA or RecBCD enzymes at high temperature, suggesting dependence on recombinational repair rather than on the RecBCD-catalyzed linear DNA degradation. Complete inhibition of growth of pta / ackA rec mutants was observed only in the presence of nearby growing cells, indicating cross-inhibition. pta rec mutants were sensitive to products of the mixed-acid fermentation of pyruvate, yet none of these substances inhibited growth of the double mutants in low-millimolar concentrations. pta , but not ackA , mutants also depend on late recombinational repair functions RuvABC or RecG. pta / ackA recF mutants are viable, suggesting, together with the inviability of pta / ackA recBC mutants, that chromosomal lesions due to the pta / ackA defect are of the double-strand-break type. We have isolated three insertional suppressors that allow slow growth of pta recBC (Ts) cells under nonpermissive conditions; all three are in or near genes with unknown functions. Although they do not form colonies, ackA rec and pta rec mutants are not killed under the nonpermissive conditions, exemplifying a case of synthetic inhibition rather than synthetic lethality." @default.
• W2019902203 created "2016-06-24" @default.
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• W2019902203 date "2005-02-15" @default.
• W2019902203 modified "2023-10-18" @default.
• W2019902203 title "A Defect in the Acetyl Coenzyme A↔Acetate Pathway Poisons Recombinational Repair-Deficient Mutants of<i>Escherichia coli</i>" @default.
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• W2019902203 doi "https://doi.org/10.1128/jb.187.4.1266-1275.2005" @default.
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