On the Nature of the Repair Deficiency in E.coli uvrE
In uvrE mutants incision is saturated at significantly lower fluences than in the isogenic parent strains. Repair of incisions is delayed and dependent on protein synthesis. As repair takes place at incision sites new dimer sites become susceptible to incision. It is suggested that in uvrE mutants the UV endonuclease complex is altered and remains bound at the site of incision.
KeywordsLower Fluences Break Closure Repair Deficiency Host Cell Reactivation Dime Site
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