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Gene expression changes in Neil1 / Neil2 / Neil3 triple knockout mouse teratoma

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE130080 | GEO | 2019/09/16

REPOSITORIES: GEO

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Gene expression changes in Neil1, Neil2 and Apex1 single knockout mouse embryonic stem cells prior and during embryoid body differentiation

Project description: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) probably due to their AP lyase activity during base excision repair (BER). 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. For comparison stem cells deficient for Apex1, the bona fide AP endonuclease during BER, were analysed in parallel.

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NEIL1 and NEIL2 DNA glycosylases protect neural crest development against mitochondrial oxidative stress

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