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首页> 外文期刊>Journal of bacteriology >Implication of the VirD4 Coupling Protein of the Lvh Type 4 Secretion System in Virulence Phenotypes of Legionella pneumophila
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Implication of the VirD4 Coupling Protein of the Lvh Type 4 Secretion System in Virulence Phenotypes of Legionella pneumophila

机译：Lvh 4型分泌系统的VirD4偶联蛋白在嗜肺军团杆菌毒力表型中的意义。

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The genome of the Philadelphia-1 strain of Legionella pneumophila, the causative organism of Legionnaires' disease, encodes two virulence-associated type 4 secretion systems (T4SSs), the Dot/Icm type 4B (T4BSS) and the Lvh type 4A (T4ASS). Broth stationary-phase cultures of most dot/icm mutants are defective in entry and evasion of phagosome acidification. However, those virulence defects can be reversed by incubating broth cultures of dot/icm mutants in water, termed water stress (WS). WS reversal requires the lvh T4ASS locus, suggesting an interaction between the two T4SSs in producing Legionella virulence phenotypes. In the current work, the loss of WS reversal in a dotA Δlvh mutant of strain JR32 was shown to be attributable to loss of the lvh virD4 gene, encoding the putative coupling protein of the T4ASS. Transformation of a dotA Δlvh mutant with virD4 also reversed entry and phagosome acidification defects in broth cultures. In addition, broth cultures of Δlvh and ΔvirD4 mutants, which were dot/icm+, showed 5-fold and >6-fold increases in translocation of the Dot/Icm translocation substrates, proteins RalF and SidD, respectively. These data demonstrate that the Lvh T4ASS functions in both broth stationary-phase cultures conventionally used for infection and cultures exposed to WS treatment. Our studies in a dotA Δlvh mutant and in a dot/icm+ background establish that VirD4 and the Lvh T4ASS contribute to virulence phenotypes and are consistent with independent functioning of Dot/Icm and Lvh T4SSs or functional substitution of the Lvh VirD4 protein for a component(s) of the Dot/Icm T4BSS.
机译：军团菌病的致病菌肺炎军团菌费城1株的基因组编码两个与毒力相关的4型分泌系统（T4SS），Dot / Icm 4B型（T4BSS）和Lvh 4A型（T4ASS）。 。大多数 dot / icm 突变体的肉汤固定相培养物在吞噬体酸化的进入和逃逸方面存在缺陷。但是，可以通过在水中孵育 dot / icm 突变体的肉汤培养物（称为水分胁迫（WS））来逆转这些毒力缺陷。 WS逆转需要 lvh T4ASS基因座，这表明两个T4SS在产生军团菌毒力表型中存在相互作用。在当前的工作中，JR32株的 dotA Δ lvh 突变体中WS逆转的丧失被证明是由于 lvh virD4 基因，编码假定的T4ASS偶联蛋白。用 virD4 转化 dotA Δ lvh 突变体也逆转了肉汤培养物中的进入和吞噬体酸化缺陷。另外， dot / icm + 的Δ lvh 和Δ virD4 突变体的肉汤培养物显示5 Dot / Icm易位底物蛋白RalF和SidD的易位分别增加了3倍和> 6倍。这些数据表明，Lvh T4ASS在常规用于感染的肉汤固定相培养物中和暴露于WS处理的培养物中均起作用。我们在 dotA Δ lvh 突变体和 dot / icm + 背景中的研究确定了VirD4和Lvh T4ASS促进了毒力表型，并且与Dot / Icm和Lvh T4SS的独立功能或Lvh VirD4蛋白的功能性替代Dot / Icm T4BSS的成分一致。

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