Disruption of cell division prevents gametogenesis in triploid Pacific oysters (Crassostrea gigas)

Triploid oysters with their large size and consistent meat quality have become a major component of the oyster aquaculture industry worldwide. It has been observed that triploid Pacific oysters (Crassostrea gigas) showed high levels of variation and sex-specific differences in sterility. Here, we analyzed mitosis and meiosis during gametogenesis in triploid Pacific oysters and the expression of key cell cycle regulatory proteins, namely members of the cyclin family (A, B, D, E). We found that in female C. gigas, expression of cyclin D and E in gonad of triploids were higher than those in diploids, while expression of cyclin A and B were significantly suppressed in the gonads of triploids. To test whether mitosis of gonia might be arrested at G1/S or S/G2 phase in triploids, we compared EdU labeling in gonadal cells of triploid and diploid oysters. The results showed a similar number of EdU-labelled cells in gonads of triploid and diploid females, indicating that gonia in triploids successfully entered the S-phase as diploids. In male triploids, gonadal expression of the four cyclin genes at the mature stage were similar to that in male diploids at the growth stage with numerous spermatogenic cells. The number of EdU-labelled cells in triploid male gonads at the mature stage was significantly more than that in diploids, suggesting more proliferating cells in triploid gonads in males. Collectively, these data inidate that the sterility of triploid females is likely caused by the failure of germ cells to enter G2-phase during mitosis. In addition, we speculate that gonadal development of triploid males was arrested at the growth stage and defective spermatogenesis might be associated with disruption of meiosis.

Automated summary

This study analyzed the expression of cell cycle regulatory proteins during gametogenesis in triploid Pacific oysters and found that differences in gene expression could explain the sterility of triploid females and the disrupted spermatogenesis in triploid males. These findings provide insights into the mechanisms underlying the sterility of triploid oysters.