(A) The effects of E(z)GLKD or ScmGLKD versus control (wGLKD) on hsGFP reporters near an active domain (dak1), inactive domain (OR67D), or PcG domains (rn, antp, or bxd) throughout the indicated stages of germ cell development. Solid line indicates mean fluorescence; shading shows one standard deviation from the mean. (B) Quantification of relative H3K27me1/2/3 antibody staining intensity in the euchromatin of control wGLKD, PclGLKD, or E(z)GLKD GSCs. (C) Quantification of reporter gene induction in GSCs in control wGLKD, PclGLKD, or E(z)GLKD. Note that PclGLKD reduces the induction of some inactive (black) and PcG (green) localized reporters but not active (magenta) localized reporters (*=p < 0.05, **=p < 0.01, N.S. = not significant; Student’s t-test, unpaired, 2-tailed). (D) Sampling model for the developmental control of silencing. In GSCs, most PRC2 is associated with Pcl, whose affinity for DNA prevents PRC2 from sampling many sites, resulting in infrequent and stochastic silencing. As Pcl levels drop during differentiation, core-PRC2, having a lower affinity for DNA, is freed to sample and silence more sites. Additionally Scm is induced and concentrated on PREs, where it preferentially concentrates residual Pcl-PRC2 through cooperativity between the Scm-PRC2 interaction and Pcl-DNA interaction.