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膜蛋白LasM促进水中[具体微生物名称未给出]的可培养性。

The Membrane Protein LasM Promotes the Culturability of in Water.

作者信息

Li Laam, Faucher Sébastien P

机构信息

Department of Natural Resource Sciences, Faculty of Agricultural and Environmental Sciences, McGill University Montreal, QC, Canada.

出版信息

Front Cell Infect Microbiol. 2016 Sep 28;6:113. doi: 10.3389/fcimb.2016.00113. eCollection 2016.

DOI:10.3389/fcimb.2016.00113
PMID:27734007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5039212/
Abstract

The water-borne pathogen strongly expresses the gene in water. This gene encodes a hypothetical protein predicted to be a membrane protein using analysis. While no conserved domains were identified in Lpg1659, similar proteins are found in many species and other aquatic bacteria. RT-qPCR showed that is positively regulated by the alternative sigma factor RpoS, which is essential for to survive in water. These observations suggest an important role of this novel protein in the survival of in water. Deletion of did not affect cell morphology, membrane integrity or tolerance to high temperature. Moreover, was dispensable for growth of in rich medium, and during infection of the amoeba and of THP-1 human macrophages. However, deletion of resulted in an early loss of culturability in water, while over-expression of this gene promoted the culturability of . Therefore, these results suggest that is required for to maintain culturability, and possibly long-term survival, in water. Since the loss of culturability observed in the absence of Lpg1659 was complemented by the addition of trace metals into water, this membrane protein is likely a transporter for acquiring essential trace metal for maintaining culturability in water and potentially in other metal-deprived conditions. Given its role in the survival of in water, Lpg1659 was named LasM for aquatic survival membrane protein.

摘要

这种水传播病原体在水中强烈表达该基因。利用分析方法,该基因编码一种预测为膜蛋白的假定蛋白。虽然在Lpg1659中未鉴定到保守结构域,但在许多物种和其他水生细菌中发现了类似的蛋白。RT-qPCR表明,该基因受替代西格玛因子RpoS的正调控,RpoS对该病原体在水中存活至关重要。这些观察结果表明这种新蛋白在该病原体于水中存活中起重要作用。缺失该基因不影响细胞形态、膜完整性或对高温的耐受性。此外,该基因对于该病原体在丰富培养基中生长以及在感染变形虫和THP-1人巨噬细胞期间是可有可无的。然而,缺失该基因导致在水中可培养性早期丧失,而该基因的过表达促进了该病原体的可培养性。因此,这些结果表明该基因是该病原体在水中维持可培养性以及可能的长期存活所必需的。由于在缺乏Lpg1659时观察到的可培养性丧失通过向水中添加微量金属得以弥补,这种膜蛋白可能是一种转运蛋白,用于获取维持水中以及可能在其他金属缺乏条件下的可培养性所需的必需微量金属。鉴于其在该病原体于水中存活中的作用,Lpg1659被命名为LasM,即嗜肺军团菌水生存活膜蛋白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/5b44db99d0e2/fcimb-06-00113-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/28deac9e9e98/fcimb-06-00113-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/c58968160328/fcimb-06-00113-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/67dcb3357730/fcimb-06-00113-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/8ecc0422e0c2/fcimb-06-00113-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/be05cc465adc/fcimb-06-00113-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/5b44db99d0e2/fcimb-06-00113-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/28deac9e9e98/fcimb-06-00113-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/c58968160328/fcimb-06-00113-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/67dcb3357730/fcimb-06-00113-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/8ecc0422e0c2/fcimb-06-00113-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/be05cc465adc/fcimb-06-00113-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da30/5039212/5b44db99d0e2/fcimb-06-00113-g0006.jpg

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