Maternal effect genes are transcribed in the oocyte and are essential for embryonic development. Few are known in mammals, but now Marisa Bartolomei and co-workers add Ctcf to this short list (see p. 2729). In vertebrates, CTCF regulates transcription at genomic loci by binding to enhancer and insulator sequences. In an earlier study into CTCF binding and activity at the maternally imprinted H19/Igf2 locus, the Bartolomei lab generated a transgenic mouse in which growing oocytes are specifically depleted of CTCF by RNAi. Using microarrays, they have now identified hundreds of genes that are misregulated in these CTCF-depleted oocytes. Most genes are downregulated; moreover, downregulated genes occur closer to CTCF-binding sites. Oocyte CTCF depletion, they report, delays not only meiosis onset but also the second, post-fertilisation division; it also perturbs zygotic genome activation, alters nuclear morphology and causes apoptotic early embryonic death. These abnormalities, further experiments show, are very likely to be a maternal effect caused by transcriptional, rather than chromatin, defects. Together, these findings reveal new and independent CTCF functions in oocyte and embryonic growth.