GSE130080
Gene expression changes in Neil1 / Neil2 / Neil3 triple knockout mouse teratoma
The bifunctional DNA glycosylases / AP lyases NEIL1 and NEIL2 excise oxidative base damages, but can also enhance the steady-state turnover of thymine DNA glycosylase (TDG) during oxidative DNA demethylation (Schomacher et al. 2016; doi:10.1038/nsmb.3151). The dual role of NEILs in antagonizing base damages and promoting epigenetic gene reactivation prompted us to investigate the consequences of NEIL deficiency during embryonic stem cell differentiation. To account for any possible functional redundancy in the NEIL family, all three paralogs NEIL1, NEIL2 and NEIL3 were inactivated using CRISPR/Cas9 in mouse embryonic stem cells. Overall design: RNA-seq gene expression profiling in teratomas derived from wildtype and Neil1 / Neil2 / Neil3 triple knockout (TKO) mouse embryonic stem cells (mESCs) in biological triplicates.