{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:04:14Z","timestamp":1792785854313,"version":"4.5.0"},"reference-count":83,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2023,4,13]],"date-time":"2023-04-13T00:00:00Z","timestamp":1681344000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Transatlantic Network of Excellence","award":["15CDV01"],"award-info":[{"award-number":["15CDV01"]}]},{"DOI":"10.13039\/501100001674","name":"Leducq Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Agence National pour la Recherche","award":["ANR-18-CE13-0011"],"award-info":[{"award-number":["ANR-18-CE13-0011"]}]},{"DOI":"10.13039\/501100002915","name":"Fondation pour la Recherche Medicale","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000272","name":"NIHR","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,9,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Haploinsufficiency of the chromo-domain protein CHD7 underlies most cases of CHARGE syndrome, a multisystem birth defect including congenital heart malformation. Context specific roles for CHD7 in various stem, progenitor, and differentiated cell lineages have been reported. Previously, we showed severe defects when Chd7 is absent from cardiopharyngeal mesoderm (CPM). Here, we investigate altered gene expression in the CPM and identify specific CHD7-bound target genes with known roles in the morphogenesis of affected structures.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>We generated conditional KO of Chd7 in CPM and analysed cardiac progenitor cells using transcriptomic and epigenomic analyses, in vivo expression analysis, and bioinformatic comparisons with existing datasets. We show CHD7 is required for correct expression of several genes established as major players in cardiac development, especially within the second heart field (SHF). We identified CHD7 binding sites in cardiac progenitor cells and found strong association with histone marks suggestive of dynamically regulated enhancers during the mesodermal to cardiac progenitor transition of mESC differentiation. Moreover, CHD7 shares a subset of its target sites with ISL1, a pioneer transcription factor in the cardiogenic gene regulatory network, including one enhancer modulating Fgf10 expression in SHF progenitor cells vs. differentiating cardiomyocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We show that CHD7 interacts with ISL1, binds ISL1-regulated cardiac enhancers, and modulates gene expression across the mesodermal heart fields during cardiac morphogenesis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvad059","type":"journal-article","created":{"date-parts":[[2023,4,13]],"date-time":"2023-04-13T11:40:53Z","timestamp":1681386053000},"page":"2089-2105","source":"Crossref","is-referenced-by-count":24,"title":["CHARGE syndrome-associated CHD7 acts at ISL1-regulated enhancers to modulate second heart field gene expression"],"prefix":"10.1093","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8579-7706","authenticated-orcid":false,"given":"Athanasia","family":"Stathopoulou","sequence":"first","affiliation":[{"name":"Developmental Biology of Birth Defects, UCL Great Ormond Street Institute of Child Health , 30 Guilford Street, London WC1N 1EH , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Genetics, Albert Einstein College of Medicine , Bronx, NY , USA"},{"name":"School of Medical Imaging, Tianjin Medical University , Tianjin , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charlotte","family":"Thellier","sequence":"additional","affiliation":[{"name":"Aix-Marseille University, CNRS UMR 7288, IBDM , Marseille , France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4357-0073","authenticated-orcid":false,"given":"Robert G","family":"Kelly","sequence":"additional","affiliation":[{"name":"Aix-Marseille University, CNRS UMR 7288, IBDM , Marseille , France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4354-5337","authenticated-orcid":false,"given":"Deyou","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Genetics, Albert Einstein College of Medicine , Bronx, NY , USA"},{"name":"Departments of Neurology and Neurosciences, Albert Einstein College of Medicine , Bronx, NY , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1487-4628","authenticated-orcid":false,"given":"Peter J","family":"Scambler","sequence":"additional","affiliation":[{"name":"Developmental Biology of Birth Defects, UCL Great Ormond Street Institute of Child 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