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SpBcl2 promotes WSSV infection by suppressing apoptotic activity of hemocytes in mud crab, Scylla paramamosain

White spot syndrome virus (WSSV) is one of the most virulent and widespread pathogens that infect almost all marine crustaceans and therefore cause huge economic losses in aquaculture. The Bcl2 protein plays a key role in the mitochondrial apoptosis pathway, which is a crucial immune response in inv...

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Bibliographic Details
Published in:Developmental and comparative immunology 2019-11, Vol.100, p.103421-103421, Article 103421
Main Authors: Chen, Jiao, Gong, Yi, Zheng, Huaiping, Ma, Hongyu, Aweya, Jude Juventus, Zhang, Yueling, Chen, Xinghan, Li, Sheng-kang
Format: Article
Language:English
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Summary:White spot syndrome virus (WSSV) is one of the most virulent and widespread pathogens that infect almost all marine crustaceans and therefore cause huge economic losses in aquaculture. The Bcl2 protein plays a key role in the mitochondrial apoptosis pathway, which is a crucial immune response in invertebrates. However, the role of Bcl2 in apoptosis and immunoregulation in mud crab, Scylla paramamosain, is poorly understood. Here, the Bcl2 homolog (SpBcl2) in S. paramamosain was cloned and its role in WSSV infection explored. The expression of SpBcl2 increased at both the transcriptional level and post-transcriptional level after WSSV infection, while the hemocytes apoptosis decreased significantly. Furthermore, there was increase in the level of cytochrome c coupled with an upregulation in the expression of SpBcl2. These results indicated that SpBcl2 suppressed apoptosis by preventing the release of cytochrome c from mitochondria, thereby promoting WSSV replication in mud crab. The findings here therefore provide novel insight into the immune response of mud crabs to WSSV infection. •The complete cDNA sequence of SpBcl2 from Scylla. paramamosain has 1122 bp in length.•SpBcl2 prevents the release of cytochrome c by modulating MOMP level.•SpBcl2 promotes WSSV infection by suppressing apoptosis in mud crabs.
ISSN:0145-305X
1879-0089
DOI:10.1016/j.dci.2019.103421