Jin Min, Chen Yanjiang, Xu Chenxi, Zhang Xiaobo
1] Key Laboratory of Conservation Biology for Endangered Wildlife of the Ministry of Education and College of Life Sciences, Zhejiang University, Hangzhou 310058, The People's Republic of China [2].
Key Laboratory of Conservation Biology for Endangered Wildlife of the Ministry of Education and College of Life Sciences, Zhejiang University, Hangzhou 310058, The People's Republic of China.
Sci Rep. 2014 Apr 28;4:4823. doi: 10.1038/srep04823.
In eukaryotes, the manipulation of the host actin cytoskeleton is a necessary strategy for viral pathogens to invade host cells. Increasing evidence indicates that the actin homolog MreB of bacteria plays key roles in cell shape formation, cell polarity, cell wall biosynthesis, and chromosome segregation. However, the role of bacterial MreB in the bacteriophage infection is not extensively investigated. To address this issue, in this study, the MreB of thermophilic Geobacillus sp. E263 from a deep-sea hydrothermal field was characterized by inhibiting the MreB polymerization and subsequently evaluating the bacteriophage GVE2 infection. The results showed that the host MreB played important roles in the bacteriophage infection at high temperature. After the host cells were treated with small molecule drug A22 or MP265, the specific inhibitors of MreB polymerization, the adsorption of GVE2 and the replication of GVE2 genome were significantly repressed. The confocal microscopy data revealed that MreB facilitated the GVE2 infection by inducing the polar distribution of virions during the phage infection. Our study contributed novel information to understand the molecular events of the host in response to bacteriophage challenge and extended our knowledge about the host-virus interaction in deep-sea vent ecosystems.
在真核生物中，操纵宿主肌动蛋白细胞骨架是病毒病原体侵入宿主细胞的必要策略。越来越多的证据表明，细菌的肌动蛋白同源物MreB在细胞形状形成、细胞极性、细胞壁生物合成和染色体分离中起关键作用。然而，细菌MreB在噬菌体感染中的作用尚未得到广泛研究。为了解决这个问题，在本研究中，通过抑制嗜热栖热放线菌MreB的聚合，随后评估噬菌体GVE2感染，对来自深海热液场的嗜热栖热放线菌E263的MreB进行了表征。结果表明，宿主MreB在高温下的噬菌体感染中起重要作用。在用小分子药物A22或MP265（MreB聚合的特异性抑制剂）处理宿主细胞后，GVE2的吸附和GVE2基因组的复制受到显著抑制。共聚焦显微镜数据显示，MreB通过在噬菌体感染期间诱导病毒粒子的极性分布促进了GVE2感染。我们的研究为理解宿主应对噬菌体挑战的分子事件提供了新信息，并扩展了我们对深海热液生态系统中宿主-病毒相互作用的认识。
