Genetic analysis of the CDI pathway from Burkholderia pseudomallei 1026b.
Genetic analysis of the CDI pathway from Burkholderia pseudomallei 1026b.
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DOI：
10.1371/journal.pone.0120265
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Low DA
中科院分区：
文献类型：
--
作者：
Koskiniemi S;Garza-Sánchez F;Edman N;Chaudhuri S;Poole SJ;Manoil C;Hayes CS;Low DA
接触依赖性生长抑制（CDI）是由CdiB/CdiA家族的双配偶体分泌系统介导的细菌间竞争模式。CdiA与易感靶细菌上的受体结合，然后递送源自其C-末端的毒素结构域。对大肠杆菌的研究表明存在多种CDI生长抑制途径，不同的系统利用不同的靶细胞蛋白来递送和激活毒素。在这里，我们探索的CDI途径在伯克霍尔德氏菌使用CDIII Bp 1026 b系统编码的染色体II类鼻疽伯克霍尔德氏菌1026 b作为一个模型。我们采取了遗传方法，并选择Burkholderia thailandensis E264突变体，这些突变体对CDIII Bp 1026 b的生长抑制具有抗性。我们鉴定了三个基因中的突变，BTH_I0359、BTH_II0599和BTH_I0986，每个基因都赋予对CDIII Bp 1026 b的抗性。BTH_I0359编码一种功能未知的小肽，而BTH_II0599编码一种预测的主要易化剂超家族的内膜转运蛋白。BTH_II0599的内膜定位表明，它可能有助于CdiA-CTII Bp 1026 b毒素从周质易位到靶细胞的细胞质中。BTH_I0986编码参与脂多糖（LPS）合成的推定的转糖基酶。BTH_I0986突变体具有改变的LPS结构，并且不与CDI+抑制剂细胞以与BTH_I0986+细胞相同的程度相互作用，表明LPS可以作为CdiAII Bp 1026 b的受体起作用。尽管CDIIIBTH_I0359、CDIIBTH_II0599和CDIIBTH_I0986突变赋予对CDIII Bp 1026 B的抗性，但它们不提供针对由B部署的CDIE 264系统的保护。thailandensis E264.总之，这些发现表明，CDI生长抑制途径是不同的，甚至在密切相关的物种之间也可能存在显着差异。
Contact-dependent growth inhibition (CDI) is a mode of inter-bacterial competition mediated by the CdiB/CdiA family of two-partner secretion systems. CdiA binds to receptors on susceptible target bacteria, then delivers a toxin domain derived from its C-terminus. Studies with Escherichia coli suggest the existence of multiple CDI growth-inhibition pathways, whereby different systems exploit distinct target-cell proteins to deliver and activate toxins. Here, we explore the CDI pathway in Burkholderia using the CDIII Bp1026b system encoded on chromosome II of Burkholderia pseudomallei 1026b as a model. We took a genetic approach and selected Burkholderia thailandensis E264 mutants that are resistant to growth inhibition by CDIII Bp1026b. We identified mutations in three genes, BTH_I0359, BTH_II0599, and BTH_I0986, each of which confers resistance to CDIII Bp1026b. BTH_I0359 encodes a small peptide of unknown function, whereas BTH_II0599 encodes a predicted inner membrane transport protein of the major facilitator superfamily. The inner membrane localization of BTH_II0599 suggests that it may facilitate translocation of CdiA-CTII Bp1026b toxin from the periplasm into the cytoplasm of target cells. BTH_I0986 encodes a putative transglycosylase involved in lipopolysaccharide (LPS) synthesis. ∆BTH_I0986 mutants have altered LPS structure and do not interact with CDI+ inhibitor cells to the same extent as BTH_I0986+ cells, suggesting that LPS could function as a receptor for CdiAII Bp1026b. Although ∆BTH_I0359, ∆BTH_II0599, and ∆BTH_I0986 mutations confer resistance to CDIII Bp1026b, they provide no protection against the CDIE264 system deployed by B. thailandensis E264. Together, these findings demonstrate that CDI growth-inhibition pathways are distinct and can differ significantly even between closely related species.
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影响因子：
4.5
作者：
Anderson MS;Garcia EC;Cotter PA
通讯作者：
Cotter PA
影响因子：
64.8
作者：
通讯作者：
--
DOI：
10.1099/00207713-48-1-317
发表时间：
1998-01-01
期刊：
INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY
影响因子：
--
作者：
Brett, PJ;DeShazer, D;Woods, DE
通讯作者：
Woods, DE
影响因子：
3.2
作者：
Aoki, S. K.;Webb, J. S.;Low, D. A.
通讯作者：
Low, D. A.
影响因子：
10.5
作者：
Diner, Elie J.;Beck, Christina M.;Hayes, Christopher S.
通讯作者：
Hayes, Christopher S.