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Here, we show that CHD8\u2010dependent chromatin licensing is required for human and mouse TSCs maintenance. CHD8 depletion impairs cell\u2010cycle progression and self\u2010renewal and selectively downregulates key stemness\u2010associated genes. In vivo, reduced placental CHD8 expression is associated with recurrent pregnancy loss in humans, and trophoblast\u2010specific deletion of\n                    <jats:italic>Chd8<\/jats:italic>\n                    in mice disrupts placentation and causes miscarriage. Mechanistically, CHD8 maintains chromatin accessibility that supports the occupancy of key trophoblast transcription factors (TFs) at their target loci and is associated with KMT2A\u2010dependent H3K4me3 deposition at TSC self\u2010renewal genes. Increasing transcription factor abundance or global H3K4me3 levels is insufficient to restore transcription in CHD8\u2010depleted cells, indicating that chromatin accessibility constitutes a dominant regulatory constraint. Together, these findings identify CHD8\u2010dependent chromatin licensing as a critical regulatory layer that sustains TSC transcriptional programs and placental development.\n                  <\/jats:p>","DOI":"10.1002\/advs.77823","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T18:00:31Z","timestamp":1790532031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CHD8\u2010Dependent Chromatin Licensing Sustains Trophoblast Stem Cell Transcriptional Programs"],"prefix":"10.1002","author":[{"given":"Yuanyuan","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology Guangdong Provincial Key Laboratory of Major Obstetric Diseases Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology Guangdong\u2010Hong Kong\u2010Macao Greater Bay Area Higher Education Joint Laboratory of Maternal\u2010Fetal Medicine The Third 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