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

ABSTRACT: It has become clear that DNA repair factors function not only in the maintenance of genomic integrity but also in active DNA demethylation and epigenetic gene regulation. This dual role raises the question if phenotypic abnormalities resulting from deficiency of DNA repair factors are due to DNA damage or impaired DNA demethylation. Here we investigate the bifunctional DNA glycosylases/lyases NEIL1 and NEIL2, which act in repair of oxidative lesions and in epigenetic demethylation.

ORGANISM(S): Mus musculus Xenopus laevis

PROVIDER: GSE130082 | GEO | 2019/09/16

REPOSITORIES: GEO

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

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). 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.

2019-09-16 | GSE130080 | GEO

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.

2019-09-16 | GSE130081 | GEO

Genome-wide analysis of gene expression in postnatal hippocampus of Neil1 and Neil2-deficient mice after hypoxia ischemia (HI)

Project description:NEIL 1-3 DNA glycosylases initiate the base excision repair pathway by removing oxidized bases from the DNA. NEIL1 and NEIL3 have been shown to protect the brain from ischemic stroke-induced injury in adult and perinatal mice, respectively. To assess the role of NEIL1 and NEIL2 in newborn mice, we used the Levine model of hypoxic-ischemic encephalopathy (HIE), modified for use in perinatal mice. We found that NEIL1 deficiency increased sensitivity to cerebral ischemia in newborn mice. In contrast, NEIL2 deficiency rendered the mice more resistant to hypoxia-ischemia. Importantly, no effect was seen in mice expressing base excision activity-deficient NEIL proteins and the global levels of the oxidative DNA lesion 5-hydroxycytosine, which is a substrate for the NEIL enzymes, did not differ significantly between the genotypes. Transcriptome analysis of NEIL1- and NEIL2-deficient hippocampus revealed changes in Neil2-deficient hippocampus that favour cell survival and limit brain injury after HI. Our data suggest a role of NEIL2 in regulating the early transcriptional stress response, critical for neuronal cell death, after brain injury. This function seems to be independent of the base excision activity of the proteins. The protective effect of NEIL2 deficiency makes NEIL2 a potential therapeutic target in treatment of perinatal HIE.

2023-12-31 | GSE236133 | GEO

Genome-wide bisulfite sequencing (GWBS) and RNA-seq in hippocampus of Neil1- and Neil2 deficient mice

Project description:We report the bisulfite sequencing and RNA-seq in hippocampus of Neil deficient adult mice. By genome-wide bisulphite sequencing (GWBS) analysis, NEIL depletion mice (including Neil1-/-, Neil2-/- and Neil1-/- Neil2-/-) consistently displayed global hypo-methylation of 5mC in base resolution in CG context, as well as in gene feature regions including transcription start sites (TSS) in CHG and CHH context by compared to wild type. RNA-seq reveals differentially expressed genes are mainly overlapped with differential methylation. A subset of overlap genes is enriched in synaptic function. Together, NEIL1 and NEIL2 functionally promote DNA methylation and impact gene expression.

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

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

| PRJNA533800 | ENA

spatial transcriptome

Project description:CA1-specific brain tissue from the hippocampal formation was isolated at baseline (homecage condition) in wildtype and NEIL1, NEIL2 or NEIL1&2-deficient mice. NEILs are DNA glycosylases potentially involved in transcription regulation. RNA was extracted and sequenced.

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

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

| PRJNA533802 | ENA

NEIL1 stimulates neurogenesis and suppresses neuroinflammation after stress

Project description:Adult neurogenesis, found in two neurogenic regions of the brain, has profound roles in neural plasticity and brain function. A hallmark feature of neurodegeneration is neuroinflammation, which can either enhance or inhibit neurogenesis depending on the context of the brain microenvironment. The consequences of deficient DNA repair in adult neurogenesis and neuroinflammation are poorly understood despite their potential relevance for homeostasis. We previously reported that loss of NEIL1, an important DNA glycosylase involved in DNA base excision repair, is associated with deficiencies in spatial memory, olfaction, and protection against ischemic stroke in mice. Here, we show that Neil1-/- mice display an anxiety-mediated behavior in the open field test, a deficient recognitive memory in novel object recognition and increased neuroinflammatory response under basal conditions. Further, mice lacking NEIL1 have decreased neurogenesis and deficient resolution of neuroinflammation following gamma irradiation (IR)-induced stress compared to WT mice. Neil1-/- IR-exposed mice also exhibit increased DNA damage and apoptosis in the hippocampus. Interestingly, behavioral tests two weeks after IR showed impaired stress response in the Neil1-/- mice. Our data indicate that NEIL1 plays an important role in adult neurogenesis and in the resolution of neuroinflammation.

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Identification of BER/SSBR proteins and the DNA glycosylases MPG, UNG2, MYH, NTH1, NEIL1 and NEIL3 in replisomes Batch 3

Project description:Base lesions in DNA can stall the replication machinery or induce mutations if bypassed. Consequently, lesions must be repaired before replication or in a post-replicative process to maintain genomic stability. Base excision repair (BER) is the main pathway for repair of base lesions, but how BER is organized during DNA replication is unclear. Here we refined the iPOND (isolation of proteins on nascent DNA) technique with targeted mass-spectrometry analysis, which enabled us to detect all proteins required for BER on nascent DNA and to monitor their spatiotemporal orchestration at replication forks. We demonstrate that XRCC1 and other BER/single-strand break repair (SSBR) proteins are enriched in replisomes in unstressed cells, supporting a cellular capacity of post-replicative BER/SSBR. Importantly, the DNA glycosylases MYH, UNG2, MPG, NTH1, NEIL1 and NEIL3 were also detected on nascent DNA. Thus our findings reveal that a broad spectrum of DNA base lesions are recognized and repaired by BER in a post-replicative process.

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