Reduced Sox2 Gene Expression Leads to Impaired Gonadal Development in Female Triploid Pacific Oyster, Crassostrea gigas

Abstract

The decreased fecundity and irregular oogenesis are commonly observed in triploid animals. However, in triploid Pacific oysters (Crassostrea gigas), females exhibit variability in reproductive capacity, with some producing abundant oocytes while others are largely infertile. Currently, the molecular mechanisms underlying these differences in triploid oysters remain poorly understood. This study investigates the role of the Sox2 transcription factor in oyster oogenesis and reproductive development. Quantitative PCR (qPCR) and in situ hybridization analysis revealed that Sox2 expression was markedly higher in the gonads of diploid females but significantly reduced in triploid females, suggesting a potential association between diminished Sox2 levels and impaired oogenesis in triploids. To test this hypothesis, RNA interference (RNAi) was used to knock down Sox2 expression in female diploids. Knockdown of Sox2 resulted in impaired gonadal development, disrupted oogenesis, and the appearance of abnormal germ cells resembling the β gonia observed in triploids. However, Sox2 knockdown did not induce apoptosis in the diploid gonadal tissue. Transcriptomic analysis revealed downregulation of genes involved in cell cycle regulation, DNA replication and repair in Sox2 knockdown C. gigas. Immunofluorescence staining of DNA damage markers showed elevated γH2AX levels in the gonads of Sox2 knockdown oysters, indicating that decreased Sox2 expression might result in defective DNA repair in germ cells of C. gigas. This study provides new insights into the molecular mechanisms underlying the sterility of triploid animals.

Keywords: Crassostrea gigas; Sox2; DNA damage; Oogenesis; Triploid.