Algoriphagus machipongonensis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA18947 | ENA |
REPOSITORIES: ENA
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Project description:E. coli K-12 BW25113 mutant strain yncC expression in biofilm cells relative to E. coli wild-type strain expression in biofilm cells. All samples were cultured in LB with glasswool at 37C for 15 hours and E. coli K-12 MG1655 mutant yncC colony cells vs wild type colony cells in LB plates 15h 37C. Quorum-sensing signal autoinducer 2 (AI-2) stimulates Escherichia coli biofilm formation through the motility regulator MqsR that induces expression of the putative transcription factor encoded by yncC. Here we show YncC increases biofilm formation by decreasing mucoidy (corroborated by decreased exopolysaccharide production and increased sensitivity to bacteriophage P1 infection). Differential gene expression and gel shift assays demonstrated that YncC is a repressor of the predicted periplasmic protein-encoding gene ybiM which was corroborated by the isogenic yncC ybiM double mutation which repressed the yncC phenotypes (biofilm formation, mucoidy, and bacteriophage resistance). Through nickel-enrichment microarrays and additional gel shift assays, we found that the putative transcription factor B3023 (directly upstream of mqsR) binds the yncC promoter. Overexpressing MqsR, AI-2 import regulators LsrR/LsrK, and AI-2 exporter TqsA induced yncC transcription whereas the AI-2 synthase LuxS and B3023 repressed yncC. MqsR has a toxic effect on E. coli bacterial growth which is partially reduced by the b3023 mutation. Therefore, AI-2 quorum-sensing control of biofilm formation is mediated through regulator MqsR that induces expression of the transcription factor YncC which serves to inhibit the expression of periplasmic YbiM; this inhibition of YbiM prevents it from overexpressing exopolysaccharide (causing mucoidy) and prevents YbiM from inhibiting biofilm formation. Keywords: biofilm gene expression and colony gene expression
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Project description:We identified the BCL6 protooncogene as a critical downstream effector of FoxO3A in self-renewal signaling of CML-initiating cells. BCL6 represses Arf and p53 in CML cells and is required for leukemia stem cell maintenance, colony formation and initiation of leukemia in transplant recipients. Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia-initiation in xenotransplanted mouse recipients. These findings identify peptide-inhibition of BCL6 as a novel strategy to eradicate leukemia-initiating cells in CML.
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