Some MEGs are expressed only in female gametes, whereas others are expressed after the embryonic genome is activated. The timing of embryonic gene activation is species-specific. In mice, embryonic gene activation occurs at the 2C stage, concurrently with the degradation of most maternal mRNA transcripts. Global expression profiles have identified distinctive patterns of maternal mRNA degradation and zygotic genome activation in mice, indicating remarkably dynamic reprogramming of gene expression at the 2C stage. One major point of inquiry was whether developmental repercussion is found in Seboxknockdown 2C embryos. In this study, Sebox-deficient MII oocytes displayed altered expression of several MEGs. First, the role of Sebox in degrading maternal factors was investigated. The degradation of maternal factors is initiated during oocyte maturation and proceeds after fertilization. To support early embryogenesis, the degradation of previously existing factors is a crucial and selective process. We measured the expression of known maternal mRNAs, all of which should be degraded in normal 2C zygotes, and found incomplete elimination of c-mos, Gbx2, and Gdf9 after Sebox RNAi knockdown. Such abnormal clearance of maternal factors likely translates to latent defects in embryonic development. Next, we confirmed the presence of abnormal ZGA and found that Mt1a, Rpl23, Ube2a and Wee1 were down-regulated after Sebox RNAi knockdown but that Cdc2, Eif1a, Hsp70.1, U2afbp-rs, and Zscan4 were not. Furthermore, expression of 4 more genes, Btg1, Klf4, Kpna1, and Muerv-1 were even up-regulated after the loss of Sebox. This finding suggests that Sebox is certainly a significant regulator of ZGA, but it is not critical or exclusive because the expression levels of 5 out of 13 genes were not affected. SEBOX contains a homeodomain and may thus act as a transcription factor. Indeed, a transcriptional activity assay confirmed a reduction of embryonic transcriptional activity after Sebox RNAi knockdown. Therefore, the regulation of ZGA by SEBOX and its control over the expression of other MEGs may occur at the transcriptional level. Further research on the GDC-0449 citations interrelationship between SEBOX as a transcriptional factor and promoters of altered MEG expression levels is required. An interesting outcome of this study was the finding that the expression levels of SCMC components were increased after Sebox RNAi knockdown. The SCMC encompasses many maternal proteins, of which FILIA, FLOPED, MATER, PADI6, and TLE6 are crucial for progression beyond the first embryonic cell division. Among these components, FLOPED, MATER, and TLE6 proteins show interactivity, whereas Filia and MATER bind directly in embryos. According to previous findings, Figla is a key regulatory molecule of Nalp5, also known as Mater, and MATER has an important role in SCMC complex formation. We confirmed a relationship between Sebox and Figla and found it noteworthy that Sebox depletion up-regulated Figla expression. These findings strongly suggest that Sebox, Figla, and SCMC components are linked. The specific interrelationships of MEGs have not been fully elucidated.