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

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

PROVIDER: PRJNA533800 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8932020.fastq.gz	Fastqsanger.gz
	SRR8932030.fastq.gz	Fastqsanger.gz
	SRR8932040.fastq.gz	Fastqsanger.gz
	SRR8932050.fastq.gz	Fastqsanger.gz
	SRR8932021.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description: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.

2019-09-16 | GSE130082 | GEO

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

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

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

Project description:Base excision repair (BER) functions 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 BER 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. Neil-deficiency in Xenopus embryos and differentiating mouse embryonic stem cells (mESCs) leads to a surprisingly restricted defect in cranial neural crest cell (cNCC) development. Neil-deficiency elicits an oxidative stress-induced TP53-dependent DNA damage response, which impairs early cNCC specification. Epistasis experiments with Tdg-deficient mESCs show no involvement of epigenetic DNA demethylation. Instead, Neil-deficiency results in oxidative damage specific to mitochondrial DNA, which triggers a TP53-mediated intrinsic apoptosis. Thus, NEIL1 and NEIL2 DNA glycosylases protect mitochondrial DNA against oxidative damage during neural crest differentiation.

| S-EPMC6768664 | biostudies-literature

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.

2024-05-01 | GSE198005 | 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

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.

2021-04-30 | GSE160621 | GEO

Gene expression changes in stage 23 Xenopus laevis embryos upon Neil2 knockdown

Project description:It was shown that neil2 is required for neural crest development in Xenopus (Schomacher et al. 2016; doi:10.1038/nsmb.3151). To gain further insights into the underlying molecular mechanism leading to neural crest defects and microcephaly in neil2 Morpholino injected Xenopus embryos, we performed RNA-seq transcriptome analysis of neil2 Morpholino versus control Morpholino injected embryos.

2019-09-16 | GSE130079 | GEO

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 and NEIL2 DNA glycosylases modulate anxiety and learning in a cooperative manner in mice.

Project description:Oxidative DNA damage in the brain has been implicated in neurodegeneration and cognitive decline. DNA glycosylases initiate base excision repair (BER), the main pathway for oxidative DNA base lesion repair. NEIL1 and NEIL3 DNA glycosylases affect cognition in mice, while the role of NEIL2 remains unclear. Here, we investigate the impact of NEIL2 and its potential overlap with NEIL1 on behavior in knockout mouse models. Neil1-/-Neil2-/- mice display hyperactivity, reduced anxiety and improved learning. Hippocampal oxidative DNA base lesion levels are comparable between genotypes and no mutator phenotype is found. Thus, impaired canonical repair is not likely to explain the altered behavior. Electrophysiology suggests reduced axonal activation in the hippocampal CA1 region in Neil1-/-Neil2-/- mice and lack of NEIL1 and NEIL2 causes dysregulation of genes in CA1 relevant for synaptic function. We postulate a cooperative function of NEIL1 and NEIL2 in genome regulation, beyond canonical BER, modulating behavior in mice.

| S-EPMC8639745 | biostudies-literature

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