<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112539/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Mus musculus</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112539</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>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)</name><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.</description><dates><publication>2018/12/06</publication></dates><accession>GSE112539</accession><cross_references><GSM>GSM3072448</GSM><GSM>GSM3072453</GSM><GSM>GSM3072452</GSM><GSM>GSM3072455</GSM><GSM>GSM3072454</GSM><GSM>GSM3072451</GSM><GSM>GSM3072450</GSM><GSM>GSM3072449</GSM><GPL>13112</GPL><SRA>SRP136807</SRA><GSE>112539</GSE><taxon>Mus musculus</taxon><PMID>[30625312]</PMID></cross_references></HashMap>