Regulation of gene expression by clay minerals
Ontology highlight
ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa PAO1
PROVIDER: GSE125524 | GEO | 2026/01/05
REPOSITORIES: GEO
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Project description:In nature, bacteria reside in biofilms - multicellular differentiated communities held together by extracellular matrix. In this work, we identified a novel subpopulation essential for biofilm formation – mineral-forming cells in Bacillus subtilis biofilms. This subpopulation contains an intracellular calcium-accumulating niche, in which the formation of a calcium carbonate mineral is initiated. As the biofilm colony develops, this mineral grows in a controlled manner, forming a functional macrostructure that serves the entire community. Consistently, biofilm development is prevented by inhibition of calcium uptake. Taken together, our results provide a clear demonstration of the orchestrated production of calcite exoskeleton, critical to morphogenesis in simple prokaryotes. We expect future research exploring this newly discovered process to shed further light on mechanisms of bacterial development.
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Project description:Bacteria can link gene expression to population density to promote group behaviors using quorum sensing. Quorum sensing controls a multitude of bacterial processes such as virulence, motility, and biofilm formation. In Vibrio fischeri, the quorum sensing-dependent transcription factor LitR inhibits biofilm formation. A previous study showed that LitR modestly inhibits transcription of the bcs locus, which comprises the genes responsible for producing the cellulose polysaccharide. However, beyond that, the mechanism of LitR’s inhibitory effect on biofilm formation was unknown. Here, we find that LitR transcriptionally activates pdeV, which encodes a c-di-GMP phosphodiesterase that indirectly promotes cleavage of the large adhesive protein LapV from the surface of V. fischeri, leading to biofilm dispersal. LitR also induces transcription of the sensor kinase VF_A1016, which we determined to be important for biofilm inhibition. Like loss of LitR, loss of VF_A1016 modestly increased bcs transcription. Through chromatin immunoprecipitation sequencing (ChIP-seq), we found that LitR directly binds to the VF_A1016 and pdeV regulatory regions. In total, we identified 147 LitR binding sites in the genome and confirmed LitR’s transcriptional control over a subset of these putative regulatory targets. Of note, we determined that LitR induces transcription of the genes encoding the diguanylate cyclase VF_1200 and the glyoxylate shunt protein AceB and inhibits expression of the putative transcription factor TfoY. LitR also differentially regulates the response regulator ArcA in static and shaking conditions. These data define the mechanism of LitR regulation of genes involved in biofilm formation and the physiology of V. fischeri.
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Project description:Biofilms with immobilized cells in industrial fermentation are beneficial. Encased in extracellular polymeric substance, cells forming biofilms are regulated by various factors. Nitric oxide (NO), as a signaling molecule, recognized as quorum sensing molecule regulating microbe biofilm formation. Regulation mechanisms of NO on bacteria biofilm have been studied extensively and deeply, while on fungus are rarely studied. In this study, we observed that low concentration of NO enhanced S. cerevisiae biofilm formation. Transcriptional and proteomic analysis revealed that transcription factor MAC1 was activated in biofilm cells under NO treatment. Overexpressed MAC1 increased yeast biofilm formation bypassing regulating the expression level of FLO11. Increased copper and iron contents in NO treated and MAC1 overexpressed cells were not responsible for increased biofilm formation. Among six downstream genes of MAC1, overexpressed CTR1 contributed yeast biofilm formation. Moreover, MAC1 and CTR1 contributed to biofilm cells ethanol resistance resulting from enhanced biofilm. The role of CTR1 protein in yeast biofilm formation may result from its hydrophobic residues in N-terminal extracellular domain. These findings suggested a NO-mediated biofilm formation mechanism that NO regulated expression levels of CTR1 through activating its transcription factor MAC1, leading enhanced biofilm formation.
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