Transgenesis of mammalian PABP reveals mRNA polyadenylation as a general stress response mechanism in bacteria.

In eukaryotes, mRNA 3'-polyadenylation triggers poly(A) binding protein (PABP) recruitment and stabilization. In a stark contrast, polyadenylation marks mRNAs for degradation in bacteria. To study this difference, we trans-express the mammalian nuclear PABPN1 chromosomally and extra-chromosomally in . Expression of PABPN1 but not the mutant PABPN1 stabilizes polyadenylated mRNAs and improves their half-lives. In the presence of PABPN1, 3'-exonuclease PNPase is not detected on PA-tailed mRNAs compromising the degradation. We show that PABPN1 trans-expression phenocopies (that encodes poly(A) polymerase, PAPI) mutation and regulates plasmid copy number. Genome-wide RNA-seq analysis shows a general up-regulation of polyadenylated mRNAs on PABPN1 expression, the largest subset of which are those involved in general stress response. However, major global stress regulators are unaffected on PABPN1 expression. Concomitantly, PABPN1 expression or mutation imparts cellular tolerance to multiple stresses. This study establishes mRNA 3'-polyadenylation as a general stress response mechanism in . .