Mutation–induced stress accelerates bacterial aging and alters the senescence phenotype

Loss-of-function mutations are often deleterious, triggering, in turn, cellular stress and complex homeostatic stress responses, called “allostasis,” to promote cell survival. We recently characterized the differential impact of deleterious single-gene deletions on Escherichia coli growth in different growth environments. We reveal how mutants reorganize their transcriptome profiles to compensate for the loss of function in a manner that reflects both the environment and the specific gene deletion. This compensation, however, is not without a cost. These mutants exhibit accelerated aging and exhibit a distinct senescence phenotype. Our results highlight the complex interplay between stress and adaptation and uncover an “aging cost” to the adaptation strategies for the individual bacterial cells.