Canonical and non-canonical PRC1 differentially contribute to regulation of neural stem cell fate

经典和非经典 PRC1 对神经干细胞命运的调控有不同的贡献

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作者:Janine Hoffmann, Theresa M Schütze, Annika Kolodziejczyk, Karolin Küster, Annekathrin Kränkel, Susanne Reinhardt, Razvan P Derihaci, Cahit Birdir, Pauline Wimberger, Haruhiko Koseki, Mareike Albert

Abstract

Neocortex development is characterized by sequential phases of neural progenitor cell (NPC) expansion, neurogenesis, and gliogenesis. Polycomb-mediated epigenetic mechanisms are known to play important roles in regulating the lineage potential of NPCs during development. The composition of Polycomb repressive complex 1 (PRC1) is highly diverse in mammals and was hypothesized to contribute to context-specific regulation of cell fate. Here, we have performed a side-by-side comparison of the role of canonical PRC1.2/1.4 and non-canonical PRC1.3/1.5, all of which are expressed in the developing neocortex, in NSC proliferation and differentiation. We found that the deletion of Pcgf2/4 in NSCs led to a strong reduction in proliferation and to altered lineage fate, both during the neurogenic and gliogenic phase, whereas Pcgf3/5 played a minor role. Mechanistically, genes encoding stem cell and neurogenic factors were bound by PRC1 and differentially expressed upon Pcgf2/4 deletion. Thus, rather than different PRC1 subcomplexes contributing to different phases of neural development, we found that canonical PRC1 played a more significant role in NSC regulation during proliferative, neurogenic, and gliogenic phases compared with non-canonical PRC1.

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