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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) [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.

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

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Neuronal development in NEIL3-deficient mice (hippocampus)

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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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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.

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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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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

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2020-01-20 | PXD016256 | Pride

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