<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/GSE318nnn/GSE318813/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318813</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>E11.5 Branchial Arches RNA-seq from controls and Ehmt1/2 neural crest knockouts</name><description>GLP and G9a repress alternative fate pathways in the neural crest. Analyses of transcript profiles from 3 control (Ehmt1+/+, Ehmt2+/+, Rosa26 TdTomato/+, Wnt1-cre) and 3 DKO (Ehmt1f/f, Ehmt2f/f, Rosa26 TdTomato/+, Wnt1-cre) E11.5 embryos demonstrated signficant upregulation of alternative fate programs in DKOs, but no observed difference in the expression of gene sets associated with cellular proliferation, apoptosis, or migration. Control embryos showed enrichment of genes associated with neural crest differentation and positive regulation of osteoblast differentiation. Alternatively, DKOs were signficantly enriched for genes associated with cardiac muscle, endothelial and myofibroblast lineages. Taken together, our RNA-seq data demonstrate that loss of GLP and G9a in the neural crest population leads to aberrant expression of alternative fate genes.</description><dates><publication>2026/08/10</publication></dates><accession>GSE318813</accession><cross_references><GSM>GSM9503649</GSM><GSM>GSM9503648</GSM><GSM>GSM9503650</GSM><GSM>GSM9503652</GSM><GSM>GSM9503651</GSM><GSM>GSM9503653</GSM><GPL>32159</GPL><GSE>318813</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>