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Résumé |
In growing cells, many mutations arise from DNA replication errors. We developed a
method to track these errors in real time in individual bacterial cells and follow
their fate, whether they are repaired or fixed as mutations. This approach allowed
us to identify the mechanism that limits error repair, providing new insight into
the origins of mutations. We also show that, within an isogenic population,
replication error repair capacity varies between cells, giving rise to a
subpopulation with transiently higher mutation rates. Such transient increases may
influence population adaptability, accelerating for instance the emergence of
antibiotic resistance. |
