KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan [CUT&TAG]

Closely related genes typically display common essential functions but also functional diversification, ensuring retention of both genes throughout evolution. The histone lysine acetyltransferases KAT6A (MOZ) and KAT6B (QKF/MORF), sharing identical protein domain structure, are mutually exclusive catalytic subunits of a multiprotein complex. Mutations in either KAT6A or KAT6B result in congenital intellectual disability disorders in human patients. In mice, loss of function of either gene results in distinct, severe phenotypic consequences. In this dataset, we investigate the effects of overexpression of KAT6B on the histone acetylation changes caused by loss of KAT6A in mouse embryonic fibroblasts. We show that Kat6b overexpression restores acetylation at histone H3 lysines 23 in Kat6a mutant mouse primary embryonic fibroblasts. CUT&Tag results detecting histone H3 lysine 23 acetylation in (H3K23ac) in primary mouse embryonic fibroblasts isolated from E14.5 Kat6a+/+Kat6b+/+, Kat6a–/–Kat6b+/+, Kat6a–/–Tg(Kat6b) and Kat6a+/+Tg(Kat6b) foetuses. N = 4 foetuses per genotype.