Abstract

Fertility decline is common in interspecific hybrids, as observed in the F 1 hybrids between the bay scallop ( Argopecten irradians irradians ) and Peruvian scallop ( A. purpuratus ). While it is known that mitochondria may regulate fertility, their role in hybrid fertility decline remains unclear. This study investigated mitochondrial ultrastructure, regulatory gene expression, and function in relation to fertility decline in F 1 hybrids. Fertility assessment revealed significant differences in fertilization rates at 30 min after fertilization between the low fertility group (Group L), the high fertility group (Group H), and the control group (self-crosses of Ai, Group N). Group L exhibited significant mitochondrial abnormalities, such as swelling, matrix vacuolization, compared to Group H and Group N. Gene expression analysis revealed significant alteration in mitochondrial regulation in hybrids, particularly the down-regulation of MFN2 (mitofusin 2) and NRF1 (nuclear respiratory factor 1) and up-regulation of DRP1 (dynamin-related protein 1), especially in Group L. Additionally, the expression of the autophagy gene ATG5 (autophagy-related gene 5) was up-regulated in Group H and down-regulated in Group L. ATP6 (ATP synthase gene) and other electron transport chain genes were significantly down-regulated in Group L. The antioxidant defense gene SOD2 (superoxide dismutase 2) expression increased in Group H but significantly decreased in Group L. Functionally, hybrids showed reduced mitochondrial membrane potential, disrupted calcium ion homeostasis, increased membrane permeability, and decreased ATP production, with the most severe impairments in Group L. These findings emphasize the possible key role of mitochondrial in the hybrid infertility of marine bivalves.