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The σ S  subunit of RNA polymerase is a master regulator of  Escherichia coli  that retards cellular senescence and bestows cells with general stress protective functions during growth arrest. We show that mutations and drugs triggering translational errors elevate σ S  levels and stability. Furthermore, mutations enhancing translational fidelity attenuate induction of the  rpoS  regulon and prevent stabilization of σ S  upon carbon starvation. Destabilization of σ S  by increased proofreading requires the presence of the σ S  recognition factor SprE (RssB) and the ClpXP protease. The data further suggest that σ S  becomes stabilized upon starvation as a result of ClpP sequestration and this sequestration is enhanced by oxidative modifications of aberrant proteins produced by erroneous translation. ClpP overproduction counteracted starvation-induced stabilization of σ S , whereas overproduction of a ClpXP substrate (ssrA-tagged GFP) stabilized σ S  in exponentially growing cells. We present a model for the sequence of events leading to the accumulation and activation of σ S  upon carbon starvation, which are linked to alterations in both ribosomal fidelity and efficiency.

genes and development

Decline in ribosomal fidelity contributes to the accumulation and stabilization of the master stress response regulator σ<sup>S</sup> upon carbon starvation

Decline in ribosomal fidelity contributes to the accumulation and stabilization of the master stress response regulator σS upon carbon starvation

Decline in ribosomal fidelity contributes to the accumulation and stabilization of the master stress response regulator σ^S upon carbon starvation