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

ABSTRACT: RNA 3'-end polyadenylation that marks transcripts for degradation is implicated in general stress response in Escherichia coli Yet, the mechanism and regulation of poly(A) polymerase I (PAPI) in stress response are obscure. We show that pcnB (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 pcnB-null mutation stabilising target mRNAs. We identify PAPI tyrosine phosphorylation at the 202 residue (Y202) that is enormously enhanced on stress exposure. This phosphorylation inhibits PAPI polyadenylation activity under stress. Consequentially, PAPI phosphodeficient mutation (tyrosine 202 to phenylalanine, Y202F) fails to stimulate mRNA expression rendering cells stress-sensitive. Bacterial tyrosine kinase Wzc phosphorylates PAPI-Y202 residue, and that wzc-null mutation renders cells stress-sensitive. Accordingly, wzc-null mutation has no effect on stress sensitivity in the presence of pcnB-null or pcnB-Y202F mutation. We also establish that PAPI phosphorylation-dependent stress tolerance mechanism is distinct and operates downstream of the primary stress regulator RpoS.

SUBMITTER: Francis N

PROVIDER: S-EPMC9764084 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature

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

Francis Nimmy N Behera Malaya R MR Natarajan Kathiresan K Laishram Rakesh S RS

Life science alliance 20221219 3

RNA 3'-end polyadenylation that marks transcripts for degradation is implicated in general stress response in <i>Escherichia coli</i> Yet, the mechanism and regulation of poly(A) polymerase I (PAPI) in stress response are obscure. We show that <i>pcnB</i> (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 PA ...[more]

PMID: 36535710

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Project description:Virulence of pathogenic bacteria is often determined by their ability to adapt to stress.The Brucella abortus general stress response (GSR) system is required for chronic mammalian infection and is regulated by phosphorylation and proteolysis.The B. abortus GSR signaling pathway has multiple layers of post-translational control and is a determinant of chronic infection.This study provides new, molecular level insight into chronic Brucella infection. Brucella spp. are adept at establishing a chronic infection in mammals. We demonstrate that core components of the ?-proteobacterial general stress response (GSR) system, PhyR and ?(E1), are required for Brucella abortus stress survival in vitro and maintenance of chronic murine infection in vivo. ?phyR and ?rpoE1 null mutants exhibit decreased survival under acute oxidative and acid stress but are not defective in infection of primary murine macrophages or in initial colonization of BALB/c mouse spleens. However, ?phyR and ?rpoE1 mutants are attenuated in spleens beginning 1 month postinfection. Thus, the B. abortus GSR system is dispensable for colonization but is required to maintain chronic infection. A genome-scale analysis of the B. abortus GSR regulon identified stress response genes previously linked to virulence and genes that affect immunomodulatory components of the cell envelope. These data support a model in which the GSR system affects both stress survival and the interface between B. abortus and the host immune system. We further demonstrate that PhyR proteolysis is a unique feature of GSR control in B. abortus. Proteolysis of PhyR provides a mechanism to avoid spurious PhyR protein interactions that inappropriately activate GSR-dependent transcription. We conclude that the B. abortus GSR system regulates acute stress adaptation and long term survival within a mammalian host and that PhyR proteolysis is a novel regulatory feature in B. abortus that ensures proper control of GSR transcription.

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

Publications

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

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