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Porin biogenesis activates the σ~E response in Salmonella hfq mutants

机译:猪源生物激活沙门氏菌hfq突变体中的σ〜E反应

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摘要

In Salmonella enterica, loss of RNA chaperon Hfq promotes proteolytic cleavage of anti-σ~E factor RseA leading to the constitutive induction of the σ~E-dependent envelope stress response. Seeking to identify the source of the inducing signal, in the present study we measured RseA cleavage and σ~E-dependent transcription in strains lacking relevant outer membrane protein (omp) genes. We found removal of the main Salmonella porin, OmpD, to markedly reduce σ~E activation in hfq mutant cells. Subsequent removal of LamB and of OmpC further attenuated the response, indicating that different OMPs collectively contribute to the σ~E-activated phenotype. Thus, loss of Hfq-mediated regulation might cause unfolded OMPs to accumulate in the periplasm, triggering the σ~E response. These findings corroborate the role of Hfq protein as a pleio-tropic regulator of OMP biogenesis in Gram-negative bacteria.
机译:在肠沙门氏菌中,RNA伴侣Hfq的缺失促进了抗σ〜E因子RseA的蛋白水解切割,从而导致了σ〜E依赖性包膜应激反应的组成型诱导。为了确定诱导信号的来源,在本研究中,我们在缺乏相关外膜蛋白(omp)基因的菌株中测量了RseA裂解和σ〜E依赖性转录。我们发现去除沙门氏菌主要蛋白OmpD可以显着降低hfq突变细胞中的σ〜E活化。随后去除LamB和OmpC进一步减弱了反应,表明不同的OMP共同参与了σ〜E激活的表型。因此,Hfq介导的调节的丧失可能导致未折叠的OMPs在周质中积累,从而触发σ〜E反应。这些发现证实了Hfq蛋白在革兰氏阴性细菌中作为OMP生物发生的多效调节剂的作用。

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