Bid-deficient fish delay grass carp reovirus (GCRV) replication and attenuate GCRV-triggered apoptosis.

Libo He,Zuoyan Zhu,Rong Huang,Lanjie Liao,Yongming Li,Yaping Wang,Lifei Luo,Hao Wang

doi:10.18632/oncotarget.19460

Libo He, Zuoyan Zhu + Show 6 more

Open Access

https://doi.org/10.18632/oncotarget.19460

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Abstract

Bid, BH3-interacting domain death agonist, is a pro-apoptotic BH3-only member of Bcl-2 family, playing an important role in apoptosis. In the study, Bid genes from grass carp (Ctenopharyngodon idellus) and rare minnow (Gobiocypris rarus), named CiBid and GrBid, were cloned and analyzed. Bid was constitutively expressed in all examined tissues of grass carp, but the expression level varied in different tissues. Following grass carp reovirus (GCRV) stimulation in vivo, Bid and apoptosis related genes Caspase-9 and Caspase-3 was up-regulated significantly at the late stage of infection. Moreover, we generated a Bid-deficient rare minnow (Bid-/-) to investigate the possible role of Bid in GCRV-triggered apoptosis. We found that the survival time of Bid-/- rare minnow after GCRV infection was extended when compared with wild-type fish, the relative copy number of GCRV in Bid-/- rare minnow was lower than that in wild-type fish, and the expression level of Caspase-9 and Caspase-3 in Bid-/- rare minnow were significantly lower than that in the wild-type fish. Collectively, the current data revealed the important role of Bid during virus-induced apoptosis in teleost fish. Our study would provide new insight into understanding the GCRV induced apoptosis and may provide a target gene for virus-resistant breeding in grass carp.

Highlights

The grass carp (Ctenopharyngodon idellus) is one of the most famous aquaculture species worldwide, accounting for 13% of global freshwater aquaculture production in 2014 [1, 2]
We found that the survival time of Bid-/- rare minnow after grass carp reovirus (GCRV) infection was extended when compared with wildtype fish, the relative copy number of GCRV in Bid-/- rare minnow was lower than that in wild-type fish, and the expression level of Caspase-9 and Caspase-3 in Bid-/rare minnow were significantly lower than that in the wild-type fish
Our results suggested that the replication of GCRV and virustriggered apoptosis were both suppressed in Bid-/- rare minnow in comparison with wild-type rare minnow

Summary

Introduction

The grass carp (Ctenopharyngodon idellus) is one of the most famous aquaculture species worldwide, accounting for 13% of global freshwater aquaculture production in 2014 [1, 2]. Frequent diseases always result in huge economic loss to the grass carp cultivation industry. Of these diseases, grass carp hemorrhage disease caused by grass carp reovirus (GCRV) has been being noticed with special concern by fish breeding scientists with the hope of disease-resistant breeding. The rare minnow (Gobiocypris rarus), a Chinese native species belonging to the family Cyprinidae, could be infected by GCRV, resulting in an up to 100% mortality rate [5]. Due to its propagational biological characteristics, rare minnow has the potential to be used as a model fish in aquatic toxicity testing, chemical safety assessment, and virus-resistant breeding [6]

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