Tyrosine phosphorylation controlled poly(A) polymerase I activity regulates general stress response in bacteria.

RNA 3'-end polyadenylation that marks transcripts for degradation is implicated in general stress response in Yet, the mechanism and regulation of poly(A) polymerase I (PAPI) in stress response are obscure. We show that (that encodes PAPI)-null mutation widely stabilises stress response mRNAs and imparts cellular tolerance to multiple stresses, whereas PAPI ectopic expression renders cells stress-sensitive. We demonstrate that there is a substantial loss of PAPI activity on stress exposure that functionally phenocopies -null mutation stabilising target mRNAs.