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Chinese giant salamander Bcl-w: An inhibitory role in iridovirus-induced mitochondrial apoptosis and virus replication

文献类型： 外文期刊

作者： Li, Yiqun 1 ; Xue, Mingyang 1 ; Dai, Yanlin 1 ; Xie, Yixing 2 ; Wei, Ying 2 ; Wang, Cheng 2 ; Tian, Mingzhu 2 ; Fan, Yuding 1 ; Jiang, Nan 1 ; Xu, Chen 1 ; Liu, Wenzhi 1 ; Meng, Yan 1 ; Zhou, Yong 1 ;

作者机构： 1.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Wudayuan Rd 8, Wuhan 430223, Peoples R China

2.Zhangjiajie Giant Salamander Natl Nat Reserve Affa, Zhangjiajie 427400, Hunan, Peoples R China

关键词： Bcl-w; Chinese giant salamander; Apoptosis; Bak; p53; Virus replication

期刊名称：VIRUS RESEARCH （ 影响因子：5.0； 五年影响因子：4.0 ）

ISSN： 0168-1702

年卷期： 2023 年 335 卷

页码：

收录情况： SCI

摘要： B-cell lymphoma-2 (BCL-2) superfamily molecules play crucial roles in mitochondrial apoptosis induced by Chinese giant salamander iridovirus (GSIV). As an anti-apoptotic molecule in the BCL-2 family, the molecular mechanism of Bcl-w during GSIV infection remains unknown. In this study, we characterized for the first time an amphibian Bcl-w from Chinese giant salamander Andrias davidianus (AdBcl-w), and its function and regulatory mechanism during GSIV infection were investigated. AdBcl-w possesses the conserved structural features of Bclw and shares 35-54% sequence identities with other Bcl-w. mRNA expression of AdBcl-w was most abundant in liver and muscle. The AdBcl-w mRNA expression was regulated during GSIV infection. Western blotting assays revealed that the level of Bcl-w protein was downregulated markedly as the infection progresses. Confocal microscopy showed that overexpressed AdBcl-w was translocated to the mitochondria after infection with GSIV. Flow cytometry analysis demonstrated that compared with control, the apoptotic progress in cells transfected with AdBcl-w was reduced while that in cells transfected with AdBcl-w siRNA was enhanced. The number of virus major capsid protein gene copies was lower and protein synthesis was reduced in AdBcl-w overexpressing cells. In addition, AdBcl-w could bind directly to the pro-apoptotic molecule AdBak, while this interaction was weakened with GSIV infection. Moreover, p53 level was reduced and the mRNA expression levels of crucial regulatory molecules in the p53 pathway were regulated in AdBcl-w overexpressing cells during GSIV infection. These results suggested that AdBcl-w inhibit GSIV replication by regulating the virus induced mitochondrial apoptosis.

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