The LetE protein enhances expression of multiple LetA/LetS-dependent transmission traits by Legionella pneumophila
The LetE protein enhances expression of multiple LetA/LetS-dependent transmission traits by Legionella pneumophila
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DOI：
10.1128/iai.72.6.3284-3293.2004
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发表时间：
2004-06-01
影响因子：
3.1
通讯作者：
Swanson, MS
中科院分区：
文献类型：
--
作者：
Bachman, MA;Swanson, MS
嗜肺军团菌定植于淡水变形虫体内，也能在肺泡巨噬细胞内复制。当它们的营养供应耗尽时，复制的细菌变得具有细胞毒性，移动性和传染性，这被认为会促进传播给新的变形虫。嗜肺乳杆菌的分化由sigma因子RpoS和FliA以及双组分调节因子LetA/LetS协调，并由letE位点增强。在这里，我们证明letE通过增加鞭毛蛋白基因flaA的表达来促进运动，但对鞭毛sigma因子基因fliA的转录几乎没有影响。除了促进运动性外，letE还诱导了静止期嗜肺乳杆菌的特征形状、色素和耐热性。为了深入了解letE如何促进传递表型的表达，我们设计了分子遗传学实验来区分以下三种模型：letE突变在milX上是极性的；letE编码一种新的小蛋白质；或者，与CsrA类似，WE编码一种调控RNA，隔离CsrA以减轻抑制。我们报道，letE编码一种激活蛋白，因为它不补充大肠杆菌csrB突变体，它指导类似于12 kda多肽的合成，而letE无义突变消除了功能。单顺反子letE RNA在指数期丰富，其在固定期的衰变需要RpoS和LetA/ let。我们还讨论了LetE蛋白如何与LetA/LetS和CsrA相互作用以增强嗜肺乳杆菌向可传播形式的分化。
Legionella pneumophila colonizes freshwater amoebae and can also replicate within alveolar macrophages. When their nutrient supply is exhausted, replicating bacteria become cytotoxic, motile, and infectious, which is thought to promote transmission to a new amoeba. The differentiation of L. pneumophila is coordinated by the sigma factors RpoS and FliA and the two-component regulator LetA/LetS and is enhanced by the letE locus. Here we demonstrate that letE promotes motility by increasing expression of the flagellin gene flaA but has little impact on the transcription of fliA, the flagellar sigma factor gene. In addition to promoting motility, letE induces the characteristic shape, pigment, and heat resistance of stationary-phase L. pneumophila. To gain insight into how letE promotes the expression of the transmission phenotype, we designed molecular genetic experiments to discriminate between the following three models: letE mutations are polar on milX; letE encodes a small novel protein; or, by analogy to csrB, WE encodes a regulatory RNA that sequesters CsrA to relieve repression. We report that letE encodes an activator protein, as it does not complement an Escherichia coli csrB mutant, it directs the synthesis of an similar to12-kDa polypeptide, and a letE nonsense mutation eliminates function. A monocistronic letE RNA is abundant during the exponential phase, and its decay during the stationary phase requires RpoS and LetA/LetS. We also discuss how the LetE protein may interact with LetA/LetS and CsrA to enhance L. pneumophilia differentiation to a transmissible form.