YdiV: a dual function protein that targets FlhDC for ClpXP-dependent degradation by promoting release of DNA-bound FlhDC complex.

YdiV: a dual function protein that targets FlhDC for ClpXP-dependent degradation by promoting release of DNA-bound FlhDC complex.
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DOI:
10.1111/j.1365-2958.2012.08007.x
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发表时间:
2012-03
影响因子:
3.6
通讯作者:
Hughes KT
Hughes KT
中科院分区:
生物学2区
文献类型:
--
作者:
Takaya A;Erhardt M;Karata K;Winterberg K;Yamamoto T;Hughes KT

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YdiV 是一种类似 EAL 的蛋白,在肠沙门氏菌中充当鞭毛主转录激活因子复合物 FlhD4C2 的转录后负调节因子,将鞭毛基因表达与营养可用性结合起来。 ClpXP 蛋白酶缺陷的突变体在中等 YdiV 表达条件下不再表现出对 FlhD4C2 依赖性转录的 YdiV 依赖性抑制。 ClpXP 蛋白酶降解 FlhD4C2,并且这种降解在 YdiV 存在的情况下会加速。 YdiV 与游离和 DNA 结合的 FlhD4C2 形成复合物;并从 DNA 中去除 FlhD4C2。 FlhD 中的 L22H 取代被分离为对 YdiV 抑制不敏感。 FlhD L22H 取代阻止了 YdiV 与游离 FlhD4C2 的相互作用以及 YdiV 释放与 DNA 结合的 FlhD4C2 的能力。这些结果表明,YdiV 阻止 FlhD4C2 依赖性鞭毛基因转录,并​​充当假定的接头以靶向 FlhD4C2 进行 ClpXP 依赖性蛋白水解。我们的结果表明,YdiV 是一种类似 EAL 的蛋白,它已从双环 GMP 磷酸二酯酶进化为双功能调节蛋白,将鞭毛基因表达与营养饥饿联系起来。
YdiV is an EAL-like protein that acts as a post-transcriptional, negative regulator of the flagellar master transcriptional activator complex, FlhD4C2, in Salmonella enterica to couple flagellar gene expression to nutrient availability. Mutants defective in ClpXP protease no longer exhibit YdiV-dependent inhibition of FlhD4C2-dependent transcription under moderate YdiV expression conditions. ClpXP protease degrades FlhD4C2, and this degradation is accelerated in the presence of YdiV. YdiV complexed with both free and DNA-bound FlhD4C2; and stripped FlhD4C2 from DNA. A L22H substitution in FlhD was isolated as insensitive to YdiV inhibition. The FlhD L22H substitution prevented the interaction of YdiV with free FlhD4C2 and the ability of YdiV to release FlhD4C2 bound to DNA. These results demonstrate that YdiV prevents FlhD4C2-dependent flagellar gene transcription and acts as a putative adaptor to target FlhD4C2 for ClpXP-dependent proteolysis. Our results suggest that YdiV is an EAL-like protein that has evolved from a dicyclic-GMP phosphodiesterase into a dual-function regulatory protein that connects flagellar gene expression to nutrient starvation.
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