Maternal RBPMS2 protein plays a crucial role in mouse blastocyst formation

Abstract Background Maternal factors that accumulate and stored in the cytoplasm of mature oocytes regulate preimplantation embryogenesis through many aspects, like pronuclear formation, genome reprogramming, zygotic genome activation and cell fate determination. However, most of maternal factors are still unknown. We investigated the role of the maternal protein RBPMS2 during early embryo development in mice and explored the underlying mechanisms. Methods The expression pattern of rbpms2 in mouse were analyzed by qRT-PCR and immunofluorescence staining. The effect of knockdown of RBPMS2 on embryo development was evaluated through microinjection of specific morpholino. RNA sequencing was performed for mechanistic analysis. The interaction between RBPMS2 and BMP pathway was studied using BMP inhibitor and activator. The effect of the localization of E-cadherin was determined by immunofluorescence staining. Results The maternal protein RBPMS2 is highly expressed in mouse oocytes and knockdown of RBPMS2 inhibits embryo development from the morula to blastocyst stage. Mechanically, RNA sequencing showed the differentially expressed genes were enriched in TGF-β signaling pathway. We then found embryo arrested in morula stage by adding BMP inhibitor into KSOM medium. And the morula-stage arrest defect caused by RBPMS2 knockdown was partially rescued by BMP activator. Furthermore, localization of E-cadherin in the membrane was impaired in response to knockdown of RBPMS2 or inhibition of BMP pathway. Conclusion Our study suggests that RBPMS2 activates the BMP pathway and thus influences the localization of E-cadherin, which is important for early mouse embryo development during compaction.