Abstract
Goose (Anser cygnoides) are highly broody with low egg production, and large number of granulosa cells undergo apoptosis during broodiness. Our previous study has found that miR-34c-5p was highly abundant in the ovary of goose with broodiness phenotype. However, the mechanism that miR-34c-5p regulates granulosa cells function remains unclear. Here, we demonstrated that broody goose had higher levels of miR-34c-5p than that in laying goose by qRT-PCR. The dual luciferase reporter assay showed that Bcl2 was identified as a direct target of miR-34c-5p, which could be negatively regulated by miR-34c-5p. Furthermore, over-expression of miR-34c-5p significantly increased the rate of apoptosis and slowed down the proliferation of granulosa cells by inhibiting the Bcl2 expression, whereas the opposite trend was obtained when granulosa cells were supplemented with miR-34c-5p inhibitors. In addition, Bcl2 mRNA level was lower in goose with a brooding phenotype than that in goose with an egg-laying phenotype. Taken together, the data suggested that miR-34c-5p regulated granulosa cells apoptosis and brooding behavior by targeting Bcl2, which not only contribute to reveal the potential mechanism of miR-34c-5p underlying granulosa cells apoptosis in goose, but also provides an effective strategy to reduce the incidence of broodiness and improve the egg production.