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Neuronal development in NEIL3-deficient mice (hippocampus)

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE161074 | 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) [DG]

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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.

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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.

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

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

| PRJNA732771 | ENA

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.

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Hippocampal Subregion Transcriptomic Profiles Associated with Age-Related Changes in Spatial Pattern Separation

Project description:Previous studies of age-related transcriptional changes indicate that cognitive impairments are associated with differentially expressed genes DEGs linked to defined neural systems; however, studies that examine multiple regions of the hippocampus fail to find major links between behavior and transcription in the dentate gyrus DG. The DG is implicated in pattern separation PS and exhibits multiple age-related changes that may affect PS performance. We hypothesize that an age-related decline in PS performance is associated with distinct changes in transcriptional profile, most strongly within the DG compared to other hippocampal subregions. We used a water maze beacon discrimination task to characterize PS in young 5 mo and middle-age 12 mo male F344 rats, followed by a spatial reference memory test. Middle-age rats showed consistent deficits in discriminating two identical beacons compared to young. Reference memory was not different between these two age groups. Interestingly, with increasing spatial overlap between the cues, older animals appeared to compensate for impaired PS performance though greater reliance on spatial reference memory. mRNA sequencing of hippocampal subregions DG, CA1, and CA3 indicated that the DG of middle-age rats expressed more genes correlated with PS performance. In contrast, reliance on a spatial reference memory was associated with differential expression of genes in regions CA1 and CA3. These results indicate that the beacon task is sensitive to PS impairment as early as middle-age, and distinct gene profiles are observed in neural circuits that underlie different strategies used to solve the task.

2020-05-22 | GSE140420 | GEO

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Project description:Functional alterations in medial temporal lobe structures, particularly the hippocampus, are central to age-related deficits in episodic memory. Research in aging laboratory animals has characterized physiological and cellular alterations in the hippocampus that occur in association with the presence and severity of such cognitive impairment. The current study compares alterations across hippocampal subregions by gene expression profiling in a rat model that closely mirrors individual differences in neurocognitive features of aging humans across a spectrum of outcomes, including both impaired memory and preserved function. Using mRNA profiling of the CA1, CA3 and dentate gyrus subregions, we have distinguished between gene groups and pathways related to chronological age and those specifically associated with impaired or preserved cognitive ability in aged rats. We confirmed earlier reported changes in gene groups related to inflammation and oxidative stress in multiple subregions and found these to be more associated with chronological age than cognitive function per se. The CA3 profile was best able to segregate aged impaired, aged unimpaired and young subject groups from each other. Characterization of gene changes that distinguished preserved from impaired function among the aged animals found altered expression of synaptic plasticity and neurodegenerative disease-related genes. Together these gene changes suggest recruitment of adaptive mechanisms that mediate synaptic plasticity to maintain function and structural integrity in aged unimpaired rats that does not occur in aged impaired animals.

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