Fig. 3. (A) Cryosection of a wild-type ovary. The ovary is stained with anti-Ezh2 (red; white arrow head) but not the surrounding somatic cells and follicle cells (orange arrowhead). (B) The effect of depletion of maternally inherited Ezh2 results in growth retardation even though Ezh2 transcription is restored at about the four-cell stage from the paternal allele (Fig. 1C), followed by a delayed restoration of normal H3-K27 by the 16-cell stage (Fig. 2B). The graph shows the average wet weight in grams of pups from Ezh2-depleted oocytes (blue bars) compared with pups with normal Ezh2 levels (red bars). (C) A summary of phenotypes with different mutations of Ezh2. Normal maternal inheritance of Ezh2 and one normal Ezh2 allele is necessary for normal development [based on O'Carroll et al. (O'Carroll et al., 2001) and this study]. Mice from a conventional knockout approach die early during embryogenesis, despite maternal supply of Ezh2, indicating that the embryonic Ezh2 transcript is essential for development. Mice without maternal Ezh2 supply but embryonic transcription are viable and fertile, but display a severe growth retardation until about the weaning age of 4 weeks.