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The effect of NEIL3 on CA1 DNA methylation

ABSTRACT: The effect of NEIL3 on CA1 DNA methylation

PROVIDER: PRJNA678962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13073700_1.fastq.gz	Fastqsanger.gz
	SRR13073700_2.fastq.gz	Fastqsanger.gz
	SRR13073701_1.fastq.gz	Fastqsanger.gz
	SRR13073701_2.fastq.gz	Fastqsanger.gz
	SRR13073702_1.fastq.gz	Fastqsanger.gz

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The effect of NEIL3 on CA1 DNA methylation

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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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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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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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Whole genome epigenetic sequencing on DNA from infarcted non-infarcted left ventricle of WT and NEIL3-deficient mice subjected to myocardial infarction

Project description:Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme endonuclease VIII-like 3 (NEIL3) was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 following MI in mice, especially in a fibroblast-enriched cell fraction. Neil3-/-mice showed increased mortality after MI compared to WT, caused by myocardial rupture. Epigenomic analysis suggested dysregulated myofibroblast proliferation and differentiation in Neil3-/-hearts and several differentially expressed genes were downstream targets of differentially methylated/hydroxymethylated transcriptional regulators. Furthermore, proliferation of Vimentin+ and SMA+ (myo)fibroblasts was increased in Neil3 -/-hearts following MI. We propose that NEIL3-dependent modulation of epigenetic DNA methylation regulates cardiac fibroblast proliferation and thereby controls extracellular matrix modulation after MI.

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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.

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

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