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

ABSTRACT: We did Genome wide RNA seq analysis between wild type MG1655 cells and mutant of bacterial poly(A) polymerase I (MG-pcnB null mutant). We show that pcnB-null mutation widely stabilises stress response mRNAs (>30%) and imparts cellular tolerance to multiple stresses.

ORGANISM(S): Escherichia coli

PROVIDER: GSE215029 | GEO | 2022/10/10

REPOSITORIES: GEO

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

Project description: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.

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

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

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RiboReport - Benchmarking ribosome profiling based identification of open reading frames in bacteria.

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Project description:PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor roles are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation These findings expose distinct Akt-dependent and independent tumor suppressor functions of PTEN in stromal fibroblasts and tumor cells, respectively, that can be used to guide clinical care of breast cancer patients Wild type. PtenF341V, PtenWT/null, and Pten null CDH1 positive epithelials cells of mammary ducts from 8 week old female mice were isolated by FACS, RNA was extracted and Affymetrix gene expression arrays were performed.

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A General Mechanism for the General Stress Response in Bacteria.

Project description:Bacteria have a widely conserved General Stress Response (GSR) that allows them to survive adverse environmental conditions. However, because the signaling proteins that initiate the GSR have evolved to respond to a vast range of species-specific signals, we lack a general understanding of how they are controlled. Here, we determined the molecular mechanism by which a member of the PPM family of protein serine/threonine phosphatases, RsbU, activates the GSR in B. subtilis. It was known that the phosphatase activity of RsbU is activated through interaction with a partner protein, RsbT, when it is released from a megadalton stress-sensing complex upon environmental stress, but how RsbT activates RsbU was not understood. Here we report that RsbT binds an otherwise flexible linker of RsbU to dimerize and activate its phosphatase domains through a conserved allosteric switch element. Conformational flexibility of the homologous linker was known to control activity of the E. coli GSR-activating protein (RssB), which lacks phosphatase activity and functions as a protease adapter protein, suggesting a unifying model for GSR activation across bacterial phyla. Furthermore, and as we now show, the crossing α-helical conformation of RsbU linkers in the active dimeric state is similar to that predicted for paralogous bacterial phosphatases with diverse N-terminal sensory domains, and to linkers known to control the activity of GGDEF diguanylate cyclases and histidine kinases. We propose that this shared regulatory mechanism provides a modularly exchangeable toolkit for bacteria to recognize diverse environmental signals.

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Expression Data from PtenF341V and Null Mouse Embryonic Fibroblasts

Project description:PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor mechanisms are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN that differentially alter the Akt axis in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation. These findings expose distinct Akt-dependent and independent tumor suppressor functions of PTEN in stromal fibroblasts and tumor cells, respectively, that can be used to guide clinical care of breast cancer patients Wild type, Pten null and PtenF341V primary mouse embryonic fibroblasts isolated from 13.5 day old embryos (E13.5) were cultured, RNA was extracted and Affymetrix gene expression arrays were performed.

2014-12-19 | E-GEOD-64302 | biostudies-arrayexpress

The poly(A) polymerase PAPS1 interacts with the RNA-directed DNA methylation pathway in sporophyte and pollen development [small RNA]

Project description:RNA-based processes play key roles in the regulation of eukaryotic gene expression. This includes both the processing of pre-mRNAs into mature mRNAs ready for translation and RNA-based silencing processes, such as RNA-directed DNA methylation (RdDM). Polyadenylation of pre-mRNAs is one important step in their processing and is carried out by three functionally specialized canonical nuclear poly(A) polymerases in Arabidopsis thaliana. Null-mutations in one of these, termed PAPS1, result in a male gametophytic defect. Using a fluorescence-labelling strategy, we have characterized this defect in more detail using RNA and small-RNA sequencing. In addition to global defects in expression of pollen-differentiation genes, paps1 null mutant pollen show a strong overaccumulation of transposable-element transcripts, yet a depletion of 21- and particularly 24-nucleotide long short interfering RNAs (siRNAs) and microRNAs (miRNAs) targeting the corresponding transposable elements. Double-mutant analyses support a specific functional interaction between PAPS1 and components of the RdDM pathway, as evident from strong synergistic phenotypes in mutant combinations involving paps1, but not paps2 paps4 mutations. In particular, the double mutant of paps1 and rna-dependent rna polymerase 6 (rdr6) shows a synergistic developmental phenotype disrupting the formation of the transmitting tract in the female gynoecium. Thus, our findings in A. Thaliana uncover a potentially general link between canonical poly(A) polymerases as components of mRNA processing and RdDM, reflecting an analogous interaction in fission yeast.

2019-12-31 | GSE127992 | GEO

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