GCRV-II主要外囊蛋白VP4通过VDAC2-介导的通路促进促进细胞亡
Kaiwen Zhao1, Yansong Zhang1, Zijia Yin1
1School of Life Science, Nanchang University, Nanchang 330031, China.
International journal of biological macromolecules
|December 4, 2024
概括
草复原病毒蛋白4 (VP4) 通过破坏信号传递,诱导鱼细胞的亡. 这种病毒蛋白调高了电压依赖性离子通道2 (VDAC2),促进流入和细胞死亡.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 水生动物卫生 水生动物卫生
背景情况:
- 草重生病毒 (GCRV) 导致草的显著死亡率.
- 病毒蛋白4 (VP4) 是GCRV的关键外部囊蛋白,但其精确的功能尚未完全理解.
- 了解VP4的作用对于开发GCRV对策至关重要.
研究的目的:
- 为了阐明GCRV VP4在Ctenopharyngodon idellus (CIK) 细胞中的功能.
- 研究VP4诱导的细胞损伤和细胞亡背后的分子机制.
- 为了确定GCRV感染的潜在治疗点.
主要方法:
- 用VP4转染的CIK细胞的转录组测序.
- 传输电子显微镜和共聚焦显微镜用于观察细胞变化.
- 对离子 (Ca2+) 度和线粒体膜潜力的分析.
- 基因沉默 (Knockdown) 的电压依赖的离子通道2 (VDAC2).
主要成果:
- VP4触发了细胞内网膜 (ER) 的压力,并改变了细胞内Ca2+的恒常性.
- VP4诱导线粒体膜潜在的损失,导致线粒体损伤和亡.
- 转录组分析显示,电压依赖性离子通道2 (VDAC2) 的显著上调.
- 增加的VP4表达与增加的CiVDAC2表达和亡相关;CiVDAC2倒置减轻了这些影响.
结论:
- GCRV VP4通过VDAC2-介导的信号通路诱导草细胞的亡.
- 这项研究强调了VDAC2在GCRV病原发生中的作用.
- 这些发现为预防和治疗草鱼中GCRV感染提供了洞察力.
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