Endo-siRNA deficiency results in oocyte maturation failure and apoptosis in porcine oocytes.

Abstract

Both microRNAs (miRNAs) and endogenous small interfering RNAs (endo-siRNAs) play key regulatory roles in gene expression. Some studies have demonstrated that the function of miRNA is suppressed in mouse oocytes, suggesting that endo-siRNA, not miRNA, is essential for female meiosis. This finding has yet to be confirmed in other species. In this study, by knockdown of DICER1, DROSHA and its cofactor DiGeorge syndrome critical region 8 (DGCR8) in porcine oocytes, we found that the proportion of oocytes with DICER1 deficiency that developed to meiosis II (MII) stage was significantly lower than oocytes with DROSHA and DGCR8 deficiency (39.23 versus 68.71 and 71.25% respectively; P<0.05). Oocytes lacking DROSHA and DGCR8 formed a barrel-shaped metaphase I spindle, with chromosomes tightly aligned at the metaphase plate whereas most oocytes (87%) lacking DICER1 showed spindle abnormalities during oocyte in vitro maturation. Furthermore, DICER1 deficiency also resulted in oocyte apoptosis. These results indicate that endo-siRNAs are essential for oocyte maturation in pigs.