<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18</volume><submitter>Rhodes CT</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/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.&lt;h4>Methods&lt;/h4>We removed &lt;i>Ezh2&lt;/i> in the MGE by generating &lt;i>Nkx2-1Cre;Ezh2&lt;/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.&lt;h4>Results&lt;/h4>Loss of &lt;i>Ezh2&lt;/i> increases somatostatin-expressing (SST+) and decreases parvalbumin-expressing (PV+) interneurons in the forebrain. We observe fewer MGE-derived interneurons in the first postnata</pubmed_abstract><journal>Frontiers in cellular neuroscience</journal><pagination>1334244</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10899338</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Loss of Ezh2 in the medial ganglionic eminence alters interneuron fate, cell morphology and gene expression profiles.</pubmed_title><pmcid>PMC10899338</pmcid><pubmed_authors>Sohn M</pubmed_authors><pubmed_authors>Lee S</pubmed_authors><pubmed_authors>Elisha L</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Naskar S</pubmed_authors><pubmed_authors>Rocha PP</pubmed_authors><pubmed_authors>Rhodes CT</pubmed_authors><pubmed_authors>Petros TJ</pubmed_authors><pubmed_authors>Stevenson P</pubmed_authors><pubmed_authors>Dale RK</pubmed_authors><pubmed_authors>Asokumar D</pubmed_authors><pubmed_authors>Lee DR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Loss of Ezh2 in the medial ganglionic eminence alters interneuron fate, cell morphology and gene expression profiles.</name><description>&lt;h4>Introduction&lt;/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.&lt;h4>Methods&lt;/h4>We removed &lt;i>Ezh2&lt;/i> in the MGE by generating &lt;i>Nkx2-1Cre;Ezh2&lt;/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.&lt;h4>Results&lt;/h4>Loss of &lt;i>Ezh2&lt;/i> increases somatostatin-expressing (SST+) and decreases parvalbumin-expressing (PV+) interneurons in the forebrain. We observe fewer MGE-derived interneurons in the first postnata</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2026-07-14T23:59:43.669Z</modification><creation>2025-04-06T11:01:31.668Z</creation></dates><accession>S-EPMC10899338</accession><cross_references><pubmed>38419656</pubmed><doi>10.3389/fncel.2024.1334244</doi></cross_references></HashMap>