{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["18"],"submitter":["Rhodes CT"],"pubmed_abstract":["<h4>Introduction</h4>Enhancer of zeste homolog 2 (Ezh2) is responsible for trimethylation of histone 3 at lysine 27 (H3K27me3), resulting in repression of gene expression. Here, we explore the role of Ezh2 in forebrain GABAergic interneuron development.<h4>Methods</h4>We removed <i>Ezh2</i> in the MGE by generating <i>Nkx2-1Cre;Ezh2</i> conditional knockout mice. We then characterized changes in MGE-derived interneuron fate and electrophysiological properties in juvenile mice, as well as alterations in gene expression, chromatin accessibility and histone modifications in the MGE.<h4>Results</h4>Loss of <i>Ezh2</i> increases somatostatin-expressing (SST+) and decreases parvalbumin-expressing (PV+) interneurons in the forebrain. We observe fewer MGE-derived interneurons in the first postnata"],"journal":["Frontiers in cellular neuroscience"],"pagination":["1334244"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10899338"],"repository":["biostudies-literature"],"pubmed_title":["Loss of Ezh2 in the medial ganglionic eminence alters interneuron fate, cell morphology and gene expression profiles."],"pmcid":["PMC10899338"],"pubmed_authors":["Sohn M","Lee S","Elisha L","Zhang Y","Naskar S","Rocha PP","Rhodes CT","Petros TJ","Stevenson P","Dale RK","Asokumar D","Lee DR"],"additional_accession":[]},"is_claimable":false,"name":"Loss of Ezh2 in the medial ganglionic eminence alters interneuron fate, cell morphology and gene expression profiles.","description":"<h4>Introduction</h4>Enhancer of zeste homolog 2 (Ezh2) is responsible for trimethylation of histone 3 at lysine 27 (H3K27me3), resulting in repression of gene expression. Here, we explore the role of Ezh2 in forebrain GABAergic interneuron development.<h4>Methods</h4>We removed <i>Ezh2</i> in the MGE by generating <i>Nkx2-1Cre;Ezh2</i> conditional knockout mice. We then characterized changes in MGE-derived interneuron fate and electrophysiological properties in juvenile mice, as well as alterations in gene expression, chromatin accessibility and histone modifications in the MGE.<h4>Results</h4>Loss of <i>Ezh2</i> increases somatostatin-expressing (SST+) and decreases parvalbumin-expressing (PV+) interneurons in the forebrain. We observe fewer MGE-derived interneurons in the first postnata","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-07-14T23:59:43.669Z","creation":"2025-04-06T11:01:31.668Z"},"accession":"S-EPMC10899338","cross_references":{"pubmed":["38419656"],"doi":["10.3389/fncel.2024.1334244"]}}