Bacterial type IV pili (T4P) contribute to virulence and can be rapidly extended and retracted to mediate twitching motility. T4P biogenesis, which is normally limited to the cell poles, is regulated by extracellular stimuli and internal signals such as cyclic di-GMP (c-di-GMP). The c-di-GMP–binding protein FimX interacts with the T4P assembly complex and, when intracellular c-di-GMP concentrations are low, assumes a unipolar localization and promotes T4P biogenesis. Here, we demonstrated that FimX formed a complex with the two-component system consisting of the histidine kinase PdeK and its downstream response regulator PdeR. This complex promoted T4P assembly in the phytopathogen Xanthomonas oryzae pv. oryzicola and virulence in rice. PdeK and the c-di-GMP phosphodiesterase activity of PdeR were required for the unipolar localization of FimX, leading to T4P extension. High amounts of c-di-GMP reduced the affinity of FimX for PdeR in vitro, consistent with FimX promoting T4P extension only under conditions of low c-di-GMP. We propose that low intracellular amounts of c-di-GMP created by PdeR facilitate the recruitment of FimX to the leading pole of motile cells. Our findings indicate that the PdeK-PdeR two-component system connects environmental cues to second messenger turnover, resulting in a change in the intracellular concentration of c-di-GMP that promotes T4P biogenesis and virulence.

中文翻译：

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PdeK-PdeR 双组分系统促进 FimX 的单极定位和 Xanthomonas oryzae pv 中的菌毛延伸。稻谷

细菌 IV 型菌毛 (T4P) 有助于毒力，并且可以快速伸展和缩回以调节抽搐运动。T4P 生物发生通常仅限于细胞两极，受细胞外刺激和内部信号如循环二 GMP (c-di-GMP) 的调节。c-di-GMP 结合蛋白 FimX 与 T4P 组装复合物相互作用，当细胞内 c-di-GMP 浓度低时，呈现单极定位并促进 T4P 生物发生。在这里，我们证明了 FimX 与由组氨酸激酶 PdeK 及其下游反应调节剂 PdeR 组成的双组分系统形成了一个复合物。这种复合物促进了植物病原体Xanthomonas oryzae pv中的 T4P 组装。稻谷和水稻的毒力。PdeK 和 PdeR 的 c-di-GMP 磷酸二酯酶活性是 FimX 单极定位所必需的，导致 T4P 延伸。大量的 c-di-GMP 在体外降低了 FimX 对 PdeR 的亲和力，这与 FimX 仅在低 c-di-GMP 条件下促进 T4P 延伸一致。我们建议由 PdeR 产生的低细胞内 c-di-GMP 促进 FimX 募集到运动细胞的前导极。我们的研究结果表明，PdeK-PdeR 双组分系统将环境线索与第二信使周转联系起来，导致细胞内 c-di-GMP 浓度发生变化，从而促进 T4P 生物发生和毒力。