有毒的Burkholderia物种模仿宿主活性聚合酶,以驱动基于活性的运动性
Erin L Benanti1, Catherine M Nguyen1, Matthew D Welch1
1Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
Cell
|April 11, 2015
概括
病原性细菌如Burkholderia pseudomallei使用BimA蛋白模仿宿主活性调节剂,使细胞入侵. 非致病菌株使用不同的机制,突出显示了细菌致病的各种策略.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 伯克霍尔德里亚物种会引起诸如梅里奥结核病和乳腺炎等疾病.
- 三元体自传递体BimA对于这些细菌的基于actin的移动性和传播至关重要.
- 众所周知,BimA的ortologs可以促进基于actin的运动性,宿主细胞融合和传播.
研究的目的:
- 研究来自不同Burkholderia物种的BimAortologs与宿主actin相互作用的机制.
- 为了比较BimA从致病性和非致病性Burkholderia物种的actin聚合活性.
- 了解BimA功能的差异如何影响细菌感染和传播.
主要方法:
- 对来自B. thailandensis,B. pseudomallei和B. mallei的BimA正义词进行比较分析.
- 在体外试验测试以评估actin核化,延长和捆绑.
- 显微镜可视化actin丝组织和宿主细胞融合.
主要成果:
- B. thailandensis BimA可以激活宿主Arp2/3复合体.
- B. pseudomallei 和 B. mallei BimA 模仿宿主 Ena/VASP 活性聚合酶.
- 在BimA模拟的差异导致了不同的actin丝组织和运动性,影响细胞融合效率.
结论:
- 致病性Burkholderia物种的BimA蛋白质是细菌Ena/VASP的模仿者.
- 细菌模仿不同的宿主活性蛋白聚合途径来影响感染.
- 特定的actin聚合机制的模仿是细菌病原和传播的关键因素.
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