The LovK-LovR Two-Component System Is a Regulator of the General Stress Pathway in Caulobacter crescentus

The LovK-LovR Two-Component System Is a Regulator of the General Stress Pathway in Caulobacter crescentus
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DOI:
10.1128/jb.00182-12
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发表时间:
2012-06-01
影响因子:
3.2
通讯作者:
Crosson, Sean
Crosson, Sean
中科院分区:
生物学3区
文献类型:
--
作者:
Foreman, Robert;Fiebig, Aretha;Crosson, Sean

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一组保守的调节因子控制新月柄杆菌中的一般应激反应,包括sigma(T)、其抗sigma因子NepR、抗抗sigma因子PhyR和跨膜传感器激酶PhyK。我们报道了可溶性组氨酸激酶LovK和单域反应调节因子LovR也在C. Crescentus一般应力通路。我们的遗传数据支持一个模型,其中LovK-LovR通过控制PhyR的磷酸化状态和抗-抗-IF活性在sigma(T)的上游起作用。lovK和lovR的转录通过需要sigT和phyR的机制被应激独立地激活。相反,lovK和lovR一起起作用以抑制一般应激调节子的转录。与LovK-LovR双组分系统作为一般应激途径的负调节剂的功能作用一致,lovK-lovR无效突变体在渗透应激后表现出增加的细胞存活,而lovK和lovR的协调过表达相对于野生型减弱细胞存活。值得注意的是,当lovR缺失时,lovK可以补充phyK无效突变体的转录和细胞存活缺陷。此外,在这种相同的遗传背景下,σ(T)依赖性转录响应于渗透胁迫而被激活。这一结果表明,黄素结合LOV(光,氧,或电压)组氨酸激酶有能力感知细胞质信号,除了环境信号蓝光。因此,PhyK-PhyR和LovK-LovR双组分信号系统协同调控了C. crescentus。
A conserved set of regulators control the general stress response in Caulobacter crescentus, including sigma(T), its anti-sigma factor NepR, the anti-anti-sigma factor PhyR, and the transmembrane sensor kinase PhyK. We report that the soluble histidine kinase LovK and the single-domain response regulator LovR also function within the C. crescentus general stress pathway. Our genetic data support a model in which LovK-LovR functions upstream of sigma(T) by controlling the phosphorylation state and thus anti-anti-if activity of PhyR. Transcription of lovK and lovR is independently activated by stress through a mechanism that requires sigT and phyR. Conversely, lovK and lovR function together to repress transcription of the general stress regulon. Concordant with a functional role of the LovK-LovR two-component system as a negative regulator of the general stress pathway, lovK-lovR-null mutants exhibit increased cell survival after osmotic stress, while coordinate overexpression of lovK and lovR attenuates cell survival relative to that of the wild type. Notably, lovK can complement the transcriptional and cell survival defects of a phyK-null mutant when lovR is deleted. Moreover, in this same genetic background, sigma(T)-dependent transcription is activated in response to osmotic stress. This result suggests that flavin-binding LOV (light, oxygen, or voltage) histidine kinases are competent to perceive cytoplasmic signals in addition to the environmental signal blue light. We conclude that the PhyK-PhyR and LovK-LovR two-component signaling systems coordinately regulate stress physiology in C. crescentus.