Pseudomonas aeruginosa isolates from cystic fibrosis patients are often mucoid (due to the overexpression of exopolysaccharide alginate) yet lost motility. It remains unclear about how P. aeruginosa coordinately regulates alginate production and the type IV pili‐driven twitching motility. Here we showed that sigma 22 factor (AlgT/U), an activator of alginate biosynthesis, repressed twitching motility by inhibiting the expression of pilin (PilA) through the intermediate transcriptional regulator AmrZ, which directly bound to the promoter region of pilA in both mucoid strain FRD1 and non‐mucoid strain PAO1. Four conserved AmrZ‐binding sites were found in pilA promoters among 10 P. aeruginosa strains although their entire pilA promoters had low identity. AmrZ has been reported to be essential for twitching in PAO1. We found that AmrZ was also required for twitching in mucoid FRD1, yet a high level of AmrZ inhibited twitching motility. This result was consistent with the phenomenon that twitching is frequently repressed in mucoid strains, in which the expression of AmrZ was highly activated by AlgT. Additionally, AlgT also inhibited the transcription of pilMNOP operon, which is involved in efficient pilus assembly. Our data elucidated a mechanism for how AlgT and AmrZ coordinately controlled twitching motility in P. aeruginosa.

中文翻译：

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σ因子AlgT和转录调节因子AmrZ如何抑制铜绿假单胞菌抽动运动的分子机制

来自囊性纤维化患者的铜绿假单胞菌分离物通常是粘液状的（由于胞外藻酸盐藻酸盐的过表达）而缺乏活力。铜绿假单胞菌如何协调调节藻酸盐的产生和IV型菌毛驱动的抽搐运动尚不清楚。在这里，我们显示了藻酸盐生物合成的激活因子sigma 22 factor（AlgT / U）通过中间转录调节因子AmrZ抑制菌毛蛋白（PilA）的表达来抑制抽搐运动，而后者直接与两个黏液中的pilA启动子区域结合FRD1菌株和非粘液性PAO1菌株。在10个铜绿假单胞菌菌株中的pilA启动子中发现了四个保守的AmrZ结合位点pilA启动子具有较低的身份。据报道，AmrZ对于PAO1中的抽动至关重要。我们发现，在黏液样FRD1中抽搐也需要AmrZ，但是高水平的AmrZ会抑制抽搐运动性。该结果与在粘液样菌株中经常抑制抽搐的现象是一致的，在该现象中，AlgT高度激活了AmrZ的表达。此外，AlgT还抑制pilMNOP操纵子的转录，而pilMNOP操纵子与有效的菌毛组装有关。我们的数据阐明了AlgT和AmrZ如何协调控制铜绿假单胞菌抽搐运动的机制。