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首页> 外文期刊>Journal of bacteriology >Phosphorylation of the Pseudomonas aeruginosa Response Regulator AlgR Is Essential for Type IV Fimbria-Mediated Twitching Motility
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Phosphorylation of the Pseudomonas aeruginosa Response Regulator AlgR Is Essential for Type IV Fimbria-Mediated Twitching Motility

机译：铜绿假单胞菌响应调节剂AlgR的磷酸化对于IV型菌毛介导的抽动运动至关重要。

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The response regulator AlgR is required for both alginate biosynthesis and type IV fimbria-mediated twitching motility in Pseudomonas aeruginosa. In this study, the roles of AlgR signal transduction and phosphorylation in twitching motility and biofilm formation were examined. The predicted phosphorylation site of AlgR (aspartate 54) and a second aspartate (aspartate 85) in the receiver domain of AlgR were mutated to asparagine, and mutant algR alleles were introduced into the chromosome of P. aeruginosa strains PAK and PAO1. Assays of these mutants demonstrated that aspartate 54 but not aspartate 85 of AlgR is required for twitching motility and biofilm initiation. However, strains expressing AlgR D85N were found to be hyperfimbriate, indicating that both aspartate 54 and aspartate 85 are involved in fimbrial biogenesis and function. algD mutants were observed to have wild-type twitching motility, indicating that AlgR control of twitching motility is not mediated via its role in the control of alginate biosynthesis. In vitro phosphorylation assays showed that AlgR D54N is not phosphorylated by the enteric histidine kinase CheA. These findings indicate that phosphorylation of AlgR most likely occurs at aspartate 54 and that aspartate 54 and aspartate 85 of AlgR are required for the control of the molecular events governing fimbrial biogenesis, twitching motility, and biofilm formation in P. aeruginosa.
机译：铜绿假单胞菌藻酸盐的生物合成和IV型菌毛介导的抽搐运动均需要反应调节剂AlgR。在这项研究中，AlgR信号转导和磷酸化在抽搐运动和生物膜形成中的作用进行了检查。 AlgR受体结构域中预测的AlgR（天冬氨酸54）和第二个天冬氨酸（天冬氨酸85）的磷酸化位点被突变为天冬酰胺，并且突变 algR 等位基因被引入 P染色体。铜绿假单胞菌PAK和PAO1。这些突变体的测定表明，抽搐运动性和生物膜启动需要AlgR的天冬氨酸54而不是天冬氨酸85。然而，发现表达AlgR D85N的菌株是高纤维状的，表明天冬氨酸54和天冬氨酸85都参与了纤维的生物发生和功能。观察到 algD 突变体具有野生型抽动能动性，表明AlgR对抽动能动性的控制不是通过其在藻酸盐生物合成控制中的作用而介导的。体外磷酸化分析表明，肠组氨酸激酶CheA不会将AlgR D54N磷酸化。这些发现表明，AlgR的磷酸化最有可能发生在天冬氨酸54上，并且AlmR的天冬氨酸54和天冬氨酸85是控制 P中控制纤维生物发生，抽动运动和生物膜形成的分子事件所必需的。铜绿。

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