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

Bibliographic Details
Title: Chinese giant salamander Bcl-w: An inhibitory role in iridovirus-induced mitochondrial apoptosis and virus replication
Authors: Yiqun Li, Mingyang Xue, Yanlin Dai, Yixing Xie, Ying Wei, Cheng Wang, Mingzhu Tian, Yuding Fan, Nan Jiang, Chen Xu, Wenzhi Liu, Yan Meng, Yong Zhou
Source: Virus Research, Vol 335, Iss , Pp 199196- (2023)
Publisher Information: Elsevier, 2023.
Publication Year: 2023
Collection: LCC:Microbiology
LCC:Infectious and parasitic diseases
Subject Terms: Bcl-w, Chinese giant salamander, Apoptosis, Bak, p53, Virus replication, Microbiology, QR1-502, Infectious and parasitic diseases, RC109-216
More Details: 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 Bcl-w 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1872-7492
Relation: http://www.sciencedirect.com/science/article/pii/S0168170223001582; https://doaj.org/toc/1872-7492
DOI: 10.1016/j.virusres.2023.199196
Access URL: https://doaj.org/article/4a73f6804d9247fd881dceb58fa0db7d
Accession Number: edsdoj.4a73f6804d9247fd881dceb58fa0db7d
Database: Directory of Open Access Journals
More Details
ISSN:18727492
DOI:10.1016/j.virusres.2023.199196
Published in:Virus Research
Language:English