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Aberrant epigenetic modification, including  N  6 -methylation of adenosine (m6A), has been frequently reported in embryos derived from parthenogenetic activation (PA). However, the role of  Igf2bp1  expression pattern in m6A modification and the mechanism through which  Igf2bp1  function is regulated in PA embryos remains elusive. Therefore, in this study, using si-Igf2bp1 and betaine ( N,N,N -trimethylglycine, a major methyl donor), we investigated the effect of  Igf2bp1  expression in m6A modification on the development of PA embryos. The results indicated that the down-regulation of  Igf2bp1  reduced the cleavage and blastula rates of PA embryos. Moreover, m6A expression level was markedly down-regulated following microinjection with si-Igf2bp1. However, the treatment with betaine could significantly restore the m6A level. Further bioinformatics analysis revealed  Igf2bp1  as the putative target of microRNA 670 (miR-670). Thus, to confirm this finding, mimics and inhibitor of miR-670 were microinjected into PA embryos. The results demonstrated that miR-670 inhibitor augmented the expression of  Igf2bp1  and rescued cleavage and blastula rates. In addition, the miR-670 inhibitor promoted the m6A expression level. TUNEL assay revealed a loss of expression of  Igf2bp1  induced cell apoptosis in PA embryos. Taken together, these results demonstrated that miR-670-3p functions as the regulator of  Igf2bp1  expression and plays a crucial role in PA development through m6A modification.

microRNA-670 modulates Igf2bp1 expression to regulate RNA methylation in parthenogenetic mouse embryonic development