SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development

Yurika Matsui, Mohamed Nadhir Djekidel, Katherine Lindsay, Parimal Samir, Nina Connolly, Gang Wu, Xiaoyang Yang, Yiping Fan, Beisi Xu and Jamy C. Peng ()
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Yurika Matsui: St. Jude Children’s Research Hospital
Mohamed Nadhir Djekidel: St. Jude Children’s Research Hospital
Katherine Lindsay: St. Jude Children’s Research Hospital
Parimal Samir: St. Jude Children’s Research Hospital
Nina Connolly: St. Jude Children’s Research Hospital
Gang Wu: St. Jude Children’s Research Hospital
Xiaoyang Yang: St. Jude Children’s Research Hospital
Yiping Fan: St. Jude Children’s Research Hospital
Beisi Xu: St. Jude Children’s Research Hospital
Jamy C. Peng: St. Jude Children’s Research Hospital

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract Stem cell survival versus death is a developmentally programmed process essential for morphogenesis, sizing, and quality control of genome integrity and cell fates. Cell death is pervasive during development, but its programming is little known. Here, we report that Smad nuclear interacting protein 1 (SNIP1) promotes neural progenitor cell survival and neurogenesis and is, therefore, integral to brain development. The SNIP1-depleted brain exhibits dysplasia with robust induction of caspase 9-dependent apoptosis. Mechanistically, SNIP1 regulates target genes that promote cell survival and neurogenesis, and its activities are influenced by TGFβ and NFκB signaling pathways. Further, SNIP1 facilitates the genomic occupancy of Polycomb complex PRC2 and instructs H3K27me3 turnover at target genes. Depletion of PRC2 is sufficient to reduce apoptosis and brain dysplasia and to partially restore genetic programs in the SNIP1-depleted brain in vivo. These findings suggest a loci-specific regulation of PRC2 and H3K27 marks to toggle cell survival and death in the developing brain.

Date: 2023
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DOI: 10.1038/s41467-023-40487-4

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