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.功能相近的基因通常兼具共同的必需功能与功能分化，这使得二者在进化过程中均得以保留。组蛋白赖氨酸乙酰转移酶（histone lysine acetyltransferases）KAT6A（MOZ）与KAT6B（QKF/MORF）具有完全一致的蛋白质结构域组成，二者为多蛋白复合物中互斥存在的催化亚基。人类患者中，KAT6A或KAT6B发生突变可引发先天性智力障碍病症。在小鼠模型中，任一基因的功能丧失均会导致显著且严重的表型异常。本数据集旨在探究KAT6B过表达对小鼠胚胎发育第9.5天（E9.5）中KAT6A功能丧失所诱导的基因表达变化的影响。研究结果显示，Kat6b过表达可逆转Kat6a突变小鼠胚胎中关键的基因表达异常。本研究对Kat6a/Kat6b+/+、Kat6a+/+Kat6b+/+、Kat6a/Tg(Kat6b)及Kat6a+/+Tg(Kat6b)4组各4例胚胎发育第9.5天小鼠胚胎开展了RNA测序（RNA-sequencing）。