the ARC of 22-day-old rats and after all animals in the LV-GFP injected group showed three complete estrous cycles, all the animals were exposed to a fertile male for five days. We observed that rats in which the LV-EED construct was correctly targeted to the ARC had fewer pups or failed to deliver a litter upon exposure to a fertile male (Supplementary Table 3), in contrast to the >90% fertility observed in LV-GFP-injected controls (Fig. 8d). Thus, preventing the reduction in Eed expression that occurs in the ARC at the onset of puberty compromises GnRH pulsatile release, delays the pubertal process, disrupts estrous cyclicity, reduces ovulation, and decreases fecundity. Altogether, these results are consistent with the interpretation that the onset of female puberty is controlled by a PcG-dependent repressive mechanism involving silencing of the Kiss1 gene in kisspeptin neurons of the MBH.
