KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan [RNA-seq]

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 gene expression changes caused by loss of KAT6A in mouse E9.5 embryos. We show that Kat6b overexpression reverses critical gene expression anomalies in Kat6a mutant embryos. RNA-sequencing of N= 4 Kat6a–/–Kat6b+/+, 4 Kat6a+/+Kat6b+/+, 4 Kat6a–/–Tg(Kat6b) and 4 Kat6a+/+Tg(Kat6b) E9.5 mouse embryos.