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Heterozygous mutations in the KAT6A or KAT6B gene cause human disorders with cardiac defects, but the contribution of their chromatin-adaptor proteins to development is unknown. We found that Ing5\u2212\/\u2212 mice had isolated cardiac ventricular septal defects. Ing4\u2212\/\u2212Ing5\u2212\/\u2212 embryos failed to undergo chorioallantoic fusion and arrested in development at embryonic day 8.5, displaying loss of histone H3 lysine 14 acetylation, reduction in H3 lysine 23 acetylation levels and reduced developmental gene expression. Embryonic day 12.5 Ing4+\/\u2212Ing5\u2212\/\u2212 hearts showed a paucity of epicardial cells and epicardium-derived cells, failure of myocardium compaction, and coronary vasculature defects, accompanied by reduced expression of epicardium genes. Cell adhesion gene expression and proepicardium outgrowth were defective in the ING4- and ING5-deficient state. Our findings suggest that ING4 and ING5 are essential for heart development and promote epicardium and epicardium-derived cell fates and imply mutation of the human ING5 gene as a possible cause of isolated ventricular septal defects.<\/jats:p>","DOI":"10.1242\/dev.202617","type":"journal-article","created":{"date-parts":[[2024,8,14]],"date-time":"2024-08-14T13:32:09Z","timestamp":1723642329000},"source":"Crossref","is-referenced-by-count":6,"title":["ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development"],"prefix":"10.1242","volume":"151","author":[{"given":"Sophia Y. 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