The effect of inhibition of host MreB on the infection of thermophilic phage GVE2 in high temperature environment.

The effect of inhibition of host MreB on the infection of thermophilic phage GVE2 in high temperature environment.
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高温环境下抑制宿主MreB对嗜热噬菌体GVE2感染的影响

DOI:
10.1038/srep04823
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发表时间:
2014-04-28
期刊:
影响因子:
4.6
通讯作者:
Zhang X
Zhang X
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Jin M;Chen Y;Xu C;Zhang X

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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发挥着关键作用。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,嗜热土芽孢杆菌的 MreB。来自深海热液场的 E263 的特征在于抑制 MreB 聚合,并随后评估噬菌体 GVE2 感染。结果表明,宿主MreB在高温噬菌体感染中发挥重要作用。小分子药物A22或MP265处理宿主细胞后,特异性抑制剂MreB聚合、GVE2吸附和GVE2基因组复制均受到显着抑制。共聚焦显微镜数据显示,MreB 在噬菌体感染过程中通过诱导病毒体的极性分布来促进 GVE2 感染。我们的研究提供了新的信息,以了解宿主响应噬菌体挑战的分子事件,并扩展了我们对深海喷口生态系统中宿主与病毒相互作用的了解。
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.
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