Abstract
Polycomb silencing represses gene expression and provides a molecular memory of chromatin state that is essential for animal development. We show that Drosophila female germline stem cells (GSCs) provide a powerful system for studying Polycomb silencing. GSCs have a non-canonical distribution of PRC2 activity and lack silenced chromatin like embryonic progenitors. As GSC daughters differentiate into nurse cells and oocytes, nurse cells, like embryonic somatic cells, silence genes in traditional Polycomb domains and in generally inactive chromatin. Developmentally controlled expression of two Polycomb repressive complex 2 (PRC2)-interacting proteins, Pcl and Scm, initiate silencing during differentiation. In GSCs, abundant Pcl inhibits PRC2-dependent silencing globally, while in nurse cells Pcl declines and newly induced Scm concentrates PRC2 activity on traditional Polycomb domains. Our results suggest that PRC2-dependent silencing is developmentally regulated by accessory proteins that either increase the concentration of PRC2 at target sites or inhibit the rate that PRC2 samples chromatin.
Highlights
Differentiation is the defining mechanism enabling the evolution and development of multicellular animals
Our results suggest a specific model for the establishment of Polycomb silencing in naïve precursors, and provide new insights into how Polycomb silencing has evolved to maintain its conserved function in animals such as mammals and insects
We examined the effect of E(z)GermLine-specific RNAi Knock Down (GLKD) on progenitor cells by purifying mRNA from control or E(z)GLKD ovaries where germline stem cell differentiation is blocked by the bag of marbles mutation (Kai et al, 2005; McKearin and Spradling, 1990)
Summary
Differentiation is the defining mechanism enabling the evolution and development of multicellular animals. Subsequent research revealed that Polycomb silencing is utilized by mammalian embryos and likely by all animals, and programs the differentiation of all somatic embryonic cells as well as progeny cells downstream from pleuripotent embryonic stem cells (ESCs) (Aloia et al, 2013; Montgomery et al, 2005). Despite these critical roles, the mechanisms PcG proteins use to initially recognize target sites, induce silencing, and maintain a memory of silencing in descendent cells is imperfectly understood. Learning how PcG proteins interact with their targets in PcG domains at the time cellular “memories” are initially formed is critically important to addressing these questions
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