An insulin-like growth factor homologue of Singapore grouper iridovirus modulates cell proliferation, apoptosis and enhances viral replication

Author:

Yan Yang1,Cui Huachun2,Guo Chuanyu31,Li Jun4,Huang Xiaohong1,Wei Jingguang1,Qin Qiwei1

Affiliation:

1. Key Laboratory of Tropical Marine Bio-resources and Ecology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou 510301, PR China

2. Department of Medicine, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294, USA

3. University of Chinese Academy of Sciences, Beijing, PR China

4. Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, 74 Zhongshan 2nd Road, Guangzhou 510080, PR China

Abstract

Insulin-like growth factors (IGFs) play crucial roles in regulating cell differentiation, proliferation and apoptosis. In this study, a novel IGF homologue gene (IGF-like) encoded by Singapore grouper iridovirus (SGIV) ORF062R (termed SGIV–IGF), was cloned and characterized. The coding region of SGIV–IGF is 771 bp in length, with a variable number of tandem repeats (VNTR) locus at the 3′-end. We cloned one isoform of this novel gene, 582 bp in length, containing the predicted IGF domain and 3.6 copy numbers of the 27 bp repeat unit. SGIV–IGF was an early transcribed gene during viral infection, and SGIV–IGF was distributed predominantly in the cytoplasm with a diffused granular appearance. Intriguingly, overexpression of SGIV–IGF was able to promote the growth of grouper embryonic cells (GP cells) by promoting G1/S phase transition, which was at least partially dependent on its 3′-end VNTR locus. Furthermore, viral titre assay and real-time quantitative PCR (RT-qPCR) analysis proved that SGIV–IGF could promote SGIV replication in grouper cells. In addition, overexpression of SGIV–IGF mildly facilitated apoptosis in SGIV-infected non-host fathead minnow (FHM) cells. Together, our study demonstrated a novel functional gene of SGIV which may regulate viral replication and cellular processes through multiple mechanisms that appear to be cell type-dependent.

Publisher

Microbiology Society

Subject

Virology

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