Ybx1 fine-tunes PRC2 activities to control embryonic brain development

Myron K. Evans, Yurika Matsui, Beisi Xu, Catherine Willis, Jennifer Loome, Luis Milburn, Yiping Fan, Vishwajeeth Pagala and Jamy C. Peng ()
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Myron K. Evans: St. Jude Children’s Research Hospital
Yurika Matsui: St. Jude Children’s Research Hospital
Beisi Xu: St. Jude Children’s Research Hospital
Catherine Willis: St. Jude Children’s Research Hospital
Jennifer Loome: St. Jude Children’s Research Hospital
Luis Milburn: St. Jude Children’s Research Hospital
Yiping Fan: St. Jude Children’s Research Hospital
Vishwajeeth Pagala: St. Jude Children’s Research Hospital
Jamy C. Peng: St. Jude Children’s Research Hospital

Nature Communications, 2020, vol. 11, issue 1, 1-18

Abstract: Abstract Chromatin modifiers affect spatiotemporal gene expression programs that underlie organismal development. The Polycomb repressive complex 2 (PRC2) is a crucial chromatin modifier in executing neurodevelopmental programs. Here, we find that PRC2 interacts with the nucleic acid–binding protein Ybx1. In the mouse embryo in vivo, Ybx1 is required for forebrain specification and restricting mid-hindbrain growth. In neural progenitor cells (NPCs), Ybx1 controls self-renewal and neuronal differentiation. Mechanistically, Ybx1 highly overlaps PRC2 binding genome-wide, controls PRC2 distribution, and inhibits H3K27me3 levels. These functions are consistent with Ybx1-mediated promotion of genes involved in forebrain specification, cell proliferation, or neuronal differentiation. In Ybx1-knockout NPCs, H3K27me3 reduction by PRC2 enzymatic inhibitor or genetic depletion partially rescues gene expression and NPC functions. Our findings suggest that Ybx1 fine-tunes PRC2 activities to regulate spatiotemporal gene expression in embryonic neural development and uncover a crucial epigenetic mechanism balancing forebrain–hindbrain lineages and self-renewal–differentiation choices in NPCs.

Date: 2020
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DOI: 10.1038/s41467-020-17878-y

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