During oocyte maturation, meiotic arrest and fertilisation, multiple processes – deposition of maternal transcripts and proteins, various signalling events, DNA replication, chromosome segregation and so on – must be tightly orchestrated to ensure that the resultant zygote is viable. Many of these processes require chromatin-driven modulation of transcription. Antoine Peters and colleagues (p. ) have uncovered an important role for the H3K9 methyltransferase Setdb1 in oocyte meiosis and early zygotic development. Mouse embryos depleted for maternal Setdb1 fail to progress to the blastocyst stage. In mutant oocytes, meiotic progression is impaired and multiple defects in spindle organisation and chromosome segregation can be observed. To try and understand the reason for these defects, the authors performed RNAseq analysis, finding misregulation of multiple genes with roles in cell division. Moreover, Setdb1-deficient oocytes show increased expression of multiple retrotransposons, consistent with the known role of Setdb1 in restraining retrotransposon expression in embryonic stem cells (although the families of elements regulated differ in the two contexts). Finally, the authors show that maternal Setdb1-deficient embryos suffer from similar defects in mitosis to those observed in oocyte meiosis. Thus, these data establish Setdb1 as a crucial regulator of meiotic and mitotic progression in the oocyte and early embryo.
