The small differences that we do see are marginally non-significant in the opposite direction to that predicted if error-prone DNA polymerases were responsible for the observed modulation in mutation rate (i.e., greater dinB and umuC expression in the wild-type than Δ luxS mutant: strain contrast test N =48, t 41 =2.0, P =0.056; Model 10 in Methods).
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Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell-cell interactions.
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