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Neuronal development in NEIL3-deficient mice (hippocampus) [DG]

ABSTRACT: brain tissue from Dentate Gyrus subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

ORGANISM(S): Mus musculus

PROVIDER: GSE175360 | GEO | 2021/11/25

REPOSITORIES: GEO

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Neuronal development in NEIL3-deficient mice (hippocampus) [CA1]

Project description:brain tissue from CA1 subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE175358 | GEO

Neuronal development in NEIL3-deficient mice (hippocampus) [CA3]

Project description:brain tissue from CA3 subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE175359 | GEO

Neuronal development in NEIL3-deficient mice (hippocampus)

Project description:brain tissue from all subregions (CA1, CA3, dentate gyrus) of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

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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.

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Genome-wide analysis of gene expression in brain of Neil3-deficient Alzheimer's disease mouse model

Project description:Oxidative stress generating DNA damage has been shown to be a key characteristic in Alzheimer’s disease (AD). However, how it affects the pathogenesis of AD is not yet fully understood. NEIL3 is a DNA glycosylase initiating oxidative DNA repair and with a distinct expression pattern in proliferating cells. In brain, its function has been linked to hippocampal-dependent memory and to induction of neurogenesis after stroke and in prion disease. Here, we generated a novel AD mouse model deficient for Neil3 to study the impact of impaired oxidative base lesion repair on the pathogenesis of AD. Our results demonstrate an age-dependent decrease in amyloid-β (Aβ) plaque deposition in female NEIL3-deficient AD mice. Moreover, male NEIL3-deficient AD mice show reduced neural stem cell proliferation in the adult hippocampus and impaired working memory. These effects seem to be independent of DNA repair as both sexes show increased level of oxidative base lesions in the hippocampus upon loss of NEIL3. Thus, our findings suggest a sex-dependent role of NEIL3 in the progression of AD by altering cerebral Aβ accumulation and promoting adult hippocampal neurogenesis to maintain cognitive function.

2022-11-15 | GSE197199 | 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.

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Transcriptome after spatial exploration in CA1-specific brain tissue from wildtype and NEIL3-deficient mice

Project description:CA1-specific brain tissue from the hippocampal formation was isolated at baseline (homecage condition) and after a spatial exploration paradigm ("open field") in wildtype and NEIL3-deficient mice. NEIL3 is a DNA glycosylase potentially involved in transcription regulation. RNA was extracted and sequenced. Subsequently, these results were correlated to an extracellular live recording of pyramidal cell activity ("place cell recording") in the same genotypes.

2021-11-01 | GSE148408 | GEO

neuronal development in NEIL3-deficient mice (hippocampus) [DG]

Project description:neuronal development in NEIL3-deficient mice (hippocampus) [DG]

| PRJNA732773 | ENA

Transcriptome profiling of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4

Project description:We performed high-throughput RNA sequencing to characterize possible differences in the transcriptome of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4, compared with control cells treated with a scramble version of the same antisense oligonucleotide

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Cooperation of the NEIL3 and Fanconi Anemia/BRCA Pathways in Interstrand Crosslink Repair

Project description:The NEIL3 DNA glycosylase is a base excision repair enzyme that excises bulky base lesions from DNA. Although NEIL3 has been shown to unhook interstrand crosslinks (ICL) in Xenopus extracts, how NEIL3 participants in ICL repair in human cells and its corporation with the canonical Fanconi anemia (FA)/BRCA pathway remain unclear. Here we show that the NEIL3 and the FA/BRCA pathways are non-epistatic in psoralen-ICL repair. The NEIL3 pathway is the major pathway for repairing psoralen-ICL, and the FA/BRCA pathway is only activated when NEIL3 is not present. Mechanistically, NEIL3 is recruited to psoralen-ICL in a rapid, PARP-dependent manner. Importantly, the NEIL3 pathway repairs psoralen-ICLs without generating double-strand breaks (DSBs), unlike the FA/BRCA pathway. In addition, we found that the RUVBL1/2 complex physically interact with NEIL3 and function within the NEIL3 pathway in psoralen-ICL repair. Moreover, TRAIP is important for the recruitment of NEIL3 but not FANCD2, and knockdown of TRAIP promotes FA/BRCA pathway activation. Interestingly, TRAIP is non-epistatic with both NEIL3 and FA pathways in psoralen-ICL repair, suggesting that TRAIP may function upstream of the two pathways. Taken together, the NEIL3 pathway is the major pathway to repair psoralen-ICL through a unique DSB-free mechanism in human cells.

2020-01-20 | PXD016256 | Pride

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