<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ziffra RS</submitter><funding>NIMH NIH HHS</funding><funding>NHGRI NIH HHS</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>205-213</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8494642</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>598(7879)</volume><pubmed_abstract>During mammalian development, differences in chromatin state coincide with cellular differentiation and reflect changes in the gene regulatory landscape&lt;sup>1&lt;/sup>. In the developing brain, cell fate specification and topographic identity are important for defining cell identity&lt;sup>2&lt;/sup> and confer selective vulnerabilities to neurodevelopmental disorders&lt;sup>3&lt;/sup>. Here, to identify cell-type-specific chromatin accessibility patterns in the developing human brain, we used a single-cell assay for transposase accessibility by sequencing (scATAC-seq) in primary tissue samples from the human forebrain. We applied unbiased analyses to identify genomic loci that undergo extensive cell-type- and brain-region-specific changes in accessibility during neurogenesis, and an integrative analysis</pubmed_abstract><journal>Nature</journal><pubmed_title>Single-cell epigenomics reveals mechanisms of human cortical development.</pubmed_title><pmcid>PMC8494642</pmcid><funding_grant_id>1K99 MH117165</funding_grant_id><funding_grant_id>5U41 HG002371-19</funding_grant_id><funding_grant_id>U41 HG002371</funding_grant_id><funding_grant_id>RF1 MH132662</funding_grant_id><funding_grant_id>K99 MH117165</funding_grant_id><funding_grant_id>U24 HG002371</funding_grant_id><funding_grant_id>U01 MH114825</funding_grant_id><funding_grant_id>T32 GM007175</funding_grant_id><funding_grant_id>R01 MH109907</funding_grant_id><funding_grant_id>U01 MH116438</funding_grant_id><funding_grant_id>U01 MH115747</funding_grant_id><funding_grant_id>R01 MH125516</funding_grant_id><funding_grant_id>R01 MH123178</funding_grant_id><funding_grant_id>R01 MH101221</funding_grant_id><funding_grant_id>RF1 MH121268</funding_grant_id><pubmed_authors>Ziffra RS</pubmed_authors><pubmed_authors>Nowakowski TJ</pubmed_authors><pubmed_authors>Haeussler M</pubmed_authors><pubmed_authors>Kim CN</pubmed_authors><pubmed_authors>Przytycki PF</pubmed_authors><pubmed_authors>Wilfert A</pubmed_authors><pubmed_authors>Turner TN</pubmed_authors><pubmed_authors>Pollard KS</pubmed_authors><pubmed_authors>Keough KC</pubmed_authors><pubmed_authors>Shin D</pubmed_authors><pubmed_authors>Ross JM</pubmed_authors><pubmed_authors>Kreimer A</pubmed_authors><pubmed_authors>Bogdanoff D</pubmed_authors><pubmed_authors>Casella AM</pubmed_authors><pubmed_authors>Eichler EE</pubmed_authors><pubmed_authors>Ahituv N</pubmed_authors><pubmed_authors>Ament SA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Single-cell epigenomics reveals mechanisms of human cortical development.</name><description>During mammalian development, differences in chromatin state coincide with cellular differentiation and reflect changes in the gene regulatory landscape&lt;sup>1&lt;/sup>. In the developing brain, cell fate specification and topographic identity are important for defining cell identity&lt;sup>2&lt;/sup> and confer selective vulnerabilities to neurodevelopmental disorders&lt;sup>3&lt;/sup>. Here, to identify cell-type-specific chromatin accessibility patterns in the developing human brain, we used a single-cell assay for transposase accessibility by sequencing (scATAC-seq) in primary tissue samples from the human forebrain. We applied unbiased analyses to identify genomic loci that undergo extensive cell-type- and brain-region-specific changes in accessibility during neurogenesis, and an integrative analysis</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-05-07T22:25:24.501Z</modification><creation>2025-04-19T08:25:16.537Z</creation></dates><accession>S-EPMC8494642</accession><cross_references><pubmed>34616060</pubmed><doi>10.1038/s41586-021-03209-8</doi></cross_references></HashMap>