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Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

ABSTRACT: Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

PROVIDER: PRJNA521223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8539810_1.fastq.gz	Fastqsanger.gz
	SRR8539810_2.fastq.gz	Fastqsanger.gz
	SRR8539809_1.fastq.gz	Fastqsanger.gz
	SRR8539809_2.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of gene expression in proliferative dentate gyrus (DG) nuclei of adult wild-type and KMT2D-deficient mice

Project description:We conducted genome wide transcription profiling by RNA-seq in proliferating neuronal progenitors after purifying EdU+ nuclei from micro-dissected DG of adult wild-type and KMT2D-deficient mice (Kmt2d +/Bgeo)

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Project description:The ability to avoid confusion between similar episodic memories enables organismal survival and fitness. This evolutionarily conserved differentiation process of memories as distinct representations is known as pattern separation. A central role for the entorhinal cortex->dentate gyrus (EC->DG) circuit in pattern separation is well established, but the molecular mechanisms that enable this circuit to mediate pattern separation memory is not known. Here we show the involvement in murine pattern separation memory of a unique transsynaptic protein complex formed by Cerebellin-4, Neogenin-1, and neurexins that is known to be selectively required for long-term plasticity in the EC->DG circuit. In vivo deletion of either presynaptic Cerebellin-4 in the entorhinal cortex or of postsynaptic Neogenin-1 in the dentate gyrus impairs acquisition of pattern separation memory. Thus, we describe a specific memory function for a defined molecular complex at an identified synapse, providing direct support for the hypothesis that synaptic plasticity contributes to the encoding of memory.

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iTRAQ-based proteomic analysis of dentate gyrus in temporal lobe epilepsy with hippocampal sclerosis

Project description:Temporal lobe epilepsy (TLE) is the most frequent type of focal epilepsy in adults, typically resistant to pharmacological treatment and mostly present with cognitive impairment and psychiatric comorbidities. The most common neuropathological hallmark in TLE patients is hippocampal sclerosis(HS). However, the underlying molecular mechanisms involved remain poorly characterized. Dentate gyrus(DG), one specific hippocampal subarea, structural and functional changes imply a key involvement of the DG in the development of TLE. In this study, isobaric tags for relative and absolute quantitation (iTRAQ) -based quantitative proteomic technique was performed to analysis of hippocampal DG obtained from patients with TLE-HS compared to control samples obtained from the autopsy. Our proteomic data identified 5583 proteins, of which 82 proteins were up-regulated and 90 proteins were down-regulated. Bioinformatics analysis indicated that differential expressed proteins enriched in “synaptic vesicle”, “mitochondrion”, “cell-cell adhesion”, “regulation of synaptic plasticity”, “ATP binding” and “Oxidative phosphorylation”. Protein-protein interaction network analysis found a pivotal module of 10 proteins that relate to “Oxidative phosphorylation”. This study is the first to investigate proteomic alterations in DG region of TLE-HS patients, and pave the way to better understanding of epileptogenesis mechanisms and future therapeutic intervention.

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