Maternal effect genes (MEGs) are genes whose RNA and proteins stored in the oocyte and play a crucial role in oocyte maturation, fertilisation and early embryo development until the zygotic genome is activated. Despite their crucial role a limited number of known genes are identified as MEGs. Our functional investigation of structural maintenance of chromosomes flexible hinge domain containing 1 (Smchd1), an epigenetic modifier that is important in female X chromosome inactivation and implicated in disease, revealed that it also contributes to essential maternal functions during development. Allele specific RNA-seq analysis of E9.5 embryos in which Smchd1was deleted in the oocyte, the zygote or both oocyte and zygote revealed that while either maternal or zygotic deletions resulted in a partially penetrant loss of imprinting, simultaneous deletion of both resulted in complete loss of imprinting for several imprinted clusters, similar to previously identified MEGs ZFP57and Trim28. Allele specific RRBS was carried out to understand whether maternal Smchd1 play a role in methylation at imprinted clusters. No difference was seen at germline differentially methylated regions (DMRs) suggesting that Smchd1 controls imprinting during early embryonic development through a different mechanism. We have recently found Smchd1 plays a role in long rang looping. To define the window of time to examine if this is true for maternal Smchd1, we tested when Smchd1 is absent our maternal deletion model. We discovered Smchd1 is absent between primary follicle formation during oocyte maturation to E2.5 embryos. DNA-FISH of imprinted clusters in these early stage embryos will be able to unveil whether Smchd1 play a role in higher order chromatin organisation to carry out its maternal effect functions. Identifying the mechanism of how Smchd1 controls maternal effect will provide a better understanding of embryonic development and may ultimately be useful in assisted reproductive technologies.