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CRISPR-Cas9-based editing of histone H3 arginine 17 reveals its methylation-dependent regulation of Yap signaling and early mouse embryo development (genomic DNA-seq data set)

ABSTRACT: we use rAPOBEC-XTEN-Cas9n-UGI (BE3) to introduce a point mutation (R17H) into 8 loci of Hist1H3 by a single sgRNA and a pre-stop codon into Carm1 in early mouse embryo, and both strategies resulted in developmental defects in pre-implantation embryos and fetal stages with smaller or developmental-delayed embryos. Transcriptomic analysis revealed that Yap1 and cell cycle signaling pathways were dysregulated in Carm1 pre-stop and H3R17H embryos, and Yap1 overexpression could rescue the developmental defects. Our results establish the direct regulatory relationship between Carm1-mediated site-specific histone modifications and mouse embryo development, and we also demonstrate that Hippo-Yap1 acts downstream of Carm1-mediated H3R17me2a to regulate the embryonic development and size determination.

ORGANISM(S): Mus musculus

PROVIDER: GSE112539 | GEO | 2018/12/06

REPOSITORIES: GEO

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CRISPR-Cas9-based editing of histone H3 arginine 17 reveals its methylation-dependent regulation of Yap signaling and early mouse embryo development (RNA-seq data set)

Project description:We use rAPOBEC-XTEN-Cas9n-UGI (BE3) to introduce a point mutation (R17H) into 8 loci of Hist1H3 by a single sgRNA and a pre-stop codon into Carm1 in early mouse embryo, and both strategies resulted in developmental defects in pre-implantation embryos and fetal stages with smaller or developmental-delayed embryos. Transcriptomic analysis revealed that Yap1 and cell cycle signaling pathways were dysregulated in Carm1 pre-stop and H3R17H embryos, and Yap1 overexpression could rescue the developmental defects. Our results establish the direct regulatory relationship between Carm1-mediated site-specific histone modifications and mouse embryo development, and we also demonstrate that Hippo-Yap1 acts downstream of Carm1-mediated H3R17me2a to regulate the embryonic development and size determination.

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Loss of CARM1 alters the developmental programming of Glioma stem-like cells and creates a druggable NGFR/NTRK dependency

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