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

Oncotarget
Libo HeYaping Wang

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 t...Continue Reading

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Datasets Mentioned

BETA
KX532178
and
KX532179

Methods Mentioned

BETA
electrophoresis
PCR
in vitro transcription

Software Mentioned

CiBid
ZIFIT Targeter
ORF Finder
ACT
GrBid
MrBayes
2U
BLAST

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BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis