Contribution of TAT system translocated PhoX to Campylobacter jejuni phosphate metabolism and resilience to environmental stresses.
Contribution of TAT system translocated PhoX to Campylobacter jejuni phosphate metabolism and resilience to environmental stresses.
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DOI：
10.1371/journal.pone.0026336
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Rajashekara G
中科院分区：
文献类型：
--
作者：
Drozd M;Gangaiah D;Liu Z;Rajashekara G
空肠弯曲菌是食用动物体内常见的胃肠道病原体。它通过食物的粪便污染传播，免疫功能低下的人感染更有可能导致严重的长期疾病。环境磷酸盐可能是环境适应性的重要传感器，获得细胞外磷酸盐的能力对于细菌的核心代谢反应至关重要。 PhoX 是空肠弯曲菌中唯一的碱性磷酸酶，是 TAT 转运系统的底物。碱性磷酸酶介导从磷酸有机化合物中水解去除无机磷酸盐 (Pi)，从而显着促进聚磷酸激酶 1 (ppk1) 介导的聚 P 的形成，聚 P 是一种调节细菌对应激和毒力反应的分子。同样，tatC 基因（TAT 系统的关键组成部分）的缺失会导致空肠弯曲菌出现多种表型，包括应激耐受性和体内定植降低。因此，我们在这里研究了 phoX 在聚 P 合成和 TAT 系统介导的反应中的贡献。与野生型相比，phoX 缺失突变体在稳定期的聚磷积累显着减少 (P<0.05)，表明 PhoX 是细胞内无机磷酸盐库的主要贡献者，而无机磷酸盐库对于聚磷合成至关重要。 phoX 缺失足以解决类似于先前描述的 ΔtatC 突变体缺陷的营养应激缺陷。此外，phoX 缺失突变体对某些抗菌药物的耐药性增加。 ΔphoX突变体在人肠上皮细胞内的侵袭和细胞内存活以及鸡定植方面也存在中度缺陷。此外，ΔphoX 突变体产生了增加的生物膜，可以用 1 mM 无机磷酸盐来挽救。 ΔphoX 突变体的 qRT-PCR 揭示了转录变化，表明生物膜表型增加的潜在机制。
Campylobacter jejuni is a common gastrointestinal pathogen that colonizes food animals; it is transmitted via fecal contamination of food, and infections in immune-compromised people are more likely to result in serious long-term illness. Environmental phosphate is likely an important sensor of environmental fitness and the ability to obtain extracellular phosphate is central to the bacteria's core metabolic responses. PhoX is the sole alkaline phosphatase in C. jejuni, a substrate of the TAT transport system. Alkaline phosphatases mediate the hydrolytic removal of inorganic phosphate (Pi) from phospho-organic compounds and thereby contribute significantly to the polyphosphate kinase 1 (ppk1) mediated formation of poly P, a molecule that regulates bacterial response to stresses and virulence. Similarly, deletion of the tatC gene, a key component of the TAT system, results in diverse phenotypes in C. jejuni including reduced stress tolerance and in vivo colonization. Therefore, here we investigated the contribution of phoX in poly P synthesis and in TAT-system mediated responses. The phoX deletion mutant showed significant decrease (P<0.05) in poly P accumulation in stationary phase compared to the wild-type, suggesting that PhoX is a major contributor to the inorganic phosphate pool in the cell which is essential for poly P synthesis. The phoX deletion is sufficient for a nutrient stress defect similar to the defect previously described for the ΔtatC mutant. Additionally, the phoX deletion mutant has increased resistance to certain antimicrobials. The ΔphoX mutant was also moderately defective in invasion and intracellular survival within human intestinal epithelial cells as well as in chicken colonization. Further, the ΔphoX mutant produced increased biofilm that can be rescued with 1 mM inorganic phosphate. The qRT-PCR of the ΔphoX mutant revealed transcriptional changes that suggest potential mechanisms for the increased biofilm phenotype.
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影响因子：
4.4
作者：
Gangaiah, Dharanesh;Kassem, Issmat I.;Rajashekara, Gireesh
通讯作者：
Rajashekara, Gireesh
影响因子：
6.4
作者：
KORLATH, JA;OSTERHOLM, MT;ROBINSON, RA
通讯作者：
ROBINSON, RA
影响因子：
4.9
作者：
Lin, J;Michel, LO;Zhang, QJ
通讯作者：
Zhang, QJ
影响因子：
3.2
作者：
Candon, Heather L.;Allan, Brenda J.;Gaynor, Erin C.
通讯作者：
Gaynor, Erin C.
DOI：
10.1016/j.ijfoodmicro.2008.12.031
发表时间：
2009-03-31
影响因子：
5.4
作者：
Greig, J. D.;Ravel, A.
通讯作者：
Ravel, A.