CpxRA Influences Xenorhabdus nematophila Colonization Initiation and Outgrowth in Steinernema carpocapsae Nematodes through Regulation of the nil Locus

CpxRA Influences Xenorhabdus nematophila Colonization Initiation and Outgrowth in Steinernema carpocapsae Nematodes through Regulation of the nil Locus
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DOI:
10.1128/aem.02658-08
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发表时间:
2009-06-15
影响因子:
4.4
通讯作者:
Goodrich-Blair, Heidi
Goodrich-Blair, Heidi
中科院分区:
生物学2区
文献类型:
--
作者:
Tran, Erin E. Herbert;Andersen, Aaron W.;Goodrich-Blair, Heidi

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嗜线杆菌互生定植于土壤寄生线虫的肠道,是昆虫的血液病原体。嗜线虫X.nematophila CpxRA双组分调控系统对于这两种宿主相互作用都是必要的(E.Herbert等,Appl.环境。微生物。73:7826-7836,2007)。嗜线虫X.nematophila与其线虫宿主的互惠关系包括两个阶段:一是开始阶段,少数细菌细胞在定植部位建立自己;二是长出阶段,这些细胞生长以填充空间。在这项研究中,我们表明CPX系统在这两个阶段都是必要的。嗜线虫X.nematophila Delta cpxR1对线虫的定植比其野生型亲本少,并且在部分定植的线虫中没有达到像野生型那样高的密度。为了测试Delta cpxR1宿主相互作用表型是否由于其编码I型Pilin亚单位蛋白的mrxA的过度表达,我们评估了Delta cpxR1 Delta mrxA1双重突变体的定植表型。该突变体表现出与Delta cpxR1相同的定殖缺陷,表明CpxR对mrxA的负调控在嗜线虫与宿主的相互作用中不起到可检测的作用。CpxR正向调节线虫定植所必需的nila、nilB和nilC基因的表达。在这里,我们证明了Delta cpxR1突变体的线虫定植缺陷是通过nilR的突变来提高nil基因的表达,nilR是nila、nilB和nILC的负调控因子。这些数据表明,以前在Delta cpxR1中观察到的线虫定植缺陷至少部分是由Nila、NilB和NILC的调节改变引起的。
The gammaproteobacterium Xenorhabdus nematophila mutualistically colonizes an intestinal region of a soil-dwelling nematode and is a blood pathogen of insects. The X. nematophila CpxRA two-component regulatory system is necessary for both of these host interactions (E. Herbert et al., Appl. Environ. Microbiol. 73:7826-7836, 2007). Mutualistic association of X. nematophila with its nematode host consists of two stages: initiation, where a small number of bacterial cells establish themselves in the colonization site, and outgrowth, where these cells grow to fill the space. In this study, we show that the Cpx system is necessary for both of these stages. X. nematophila Delta cpxR1 colonized fewer nematodes than its wild-type parent and did not achieve as high a density as did the wild type within a portion of the colonized nematodes. To test whether the Delta cpxR1 host interaction phenotypes are due to its overexpression of mrxA, encoding the type I pilin subunit protein, we assessed the colonization phenotype of a Delta cpxR1 Delta mrxA1 double mutant. This mutant displayed the same colonization defect as Delta cpxR1, indicating that CpxR negative regulation of mrxA does not play a detectable role in X. nematophila-host interactions. CpxR positively regulates expression of nilA, nilB, and nilC genes necessary for nematode colonization. Here we show that the nematode colonization defect of the Delta cpxR1 mutant is rescued by elevating nil gene expression through mutation of nilR, a negative regulator of nilA, nilB, and nilC. These data suggest that the nematode colonization defect previously observed in Delta cpxR1 is caused, at least in part, by altered regulation of nilA, nilB, and nilC.