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Biofilm Formation by Bacillus subtilis Requires an Endoribonuclease-containing Multisubunit Complex that Controls mRNA Levels for the Matrix Gene Repressor SinR

机译:枯草芽孢杆菌的生物膜形成需要内含核糖核酸酶的多亚基复合物该复合物控制基质基因阻遏物SinR的mRNA水平。

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摘要

Biofilm formation by Bacillus subtilis is largely governed by a circuit in which the response regulator Spo0A turns on the gene for the anti-repressor SinI. SinI, in turn, binds to and inactivates SinR, a dedicated repressor of genes for matrix production. Mutants of the genes ylbF, ymcA, and yaaT are blocked in biofilm formation, but the mechanism by which they act has been mysterious. A recent report attributed their role in biofilm formation to stimulating Spo0A activity. However, we detect no measurable effect on the transcription of sinI. Instead, we find that the block in biofilm formation is caused by an increase in the levels of SinR and of its mRNA. Evidence is presented that YlbF, YmcA and YaaT interact with, and control the activity of, RNase Y, which is known to destabilize sinR mRNA. We show that the processing of another target of RNase Y, cggR-gapA mRNA, similarly depends on YlbF and YmcA. Our work suggests that sinR mRNA stability is an additional posttranscriptional control mechanism governing the switch to multicellularity and raises the possibility that YlbF, YmcA, and YaaT broadly regulate mRNA stability as part of an RNase Y-containing, multi-subunit complex.
机译:枯草芽孢杆菌形成的生物膜主要受电路控制,在该电路中,响应调节器Spo0A开启了抗阻遏物SinI的基因。反过来,SinI与SinR结合并使其失活,SinR是用于生产基质的基因的专用阻遏物。基因ylbF,ymcA和yaaT的突变体在生物膜形成中受到阻滞,但是它们起作用的机制却是一个谜。最近的一份报告将其在生物膜形成中的作用归因于刺激Spo0A活性。但是,我们没有检测到对sinI转录的可测量的影响。相反,我们发现生物膜形成受阻是由SinR及其mRNA水平的升高引起的。证据表明,YlbF,YmcA和YaaT与RNase Y相互作用并控制其活性,而后者已知会破坏sinR mRNA的稳定性。我们表明,RNase Y的另一个靶标cggR-gapA mRNA的加工类似地取决于YlbF和YmcA。我们的工作表明,sinR mRNA稳定性是控制向多细胞性转换的另一种转录后控制机制,并增加了YlbF,YmcA和YaaT作为含有RNase Y的多亚基复合物的一部分广泛调节mRNA稳定性的可能性。

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