Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA259611 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1559360.fastq.gz | Fastqsanger.gz | |||
| SRR1559370.fastq.gz | Fastqsanger.gz | |||
| SRR1559361.fastq.gz | Fastqsanger.gz | |||
| SRR1559371.fastq.gz | Fastqsanger.gz | |||
| SRR1559362.fastq.gz | Fastqsanger.gz |
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Project description:We performed deep-sequencing analysis of small RNA extracted from neuronal progenitors at different developmental stages. The RNA samples were extracted from microdissected tissues of dorsal or lateral sub-ventricular zone (SVZ) (to analyze the immature progenitor pools), of rostral migration stream (RMS) (to analyze the migrating neuroblasts) or of olfactory bulbs (OB) (to analyze both immature and mature neurons). These tissues were dissected from animals at variable ages: P1 and P6 for SVZ samples, P15 and P28 for RMS and OB samples. Expression profile of microRNA in time and space along post-natal neurogenesis
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Project description:During cortical development, radial glial cells, known as neural stem cells, initially generate a large number of cortical glutamatergic pyramidal neurons through a process called neurogenesis. This is followed by the generation of a diversity of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, known as gliogenesis. However, the molecular mechanisms underlying the switch from cortical neurogenesis to gliogenesis, and the subsequent fate determination of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, remain unclear. Here, we report that extracellular signal-regulated kinase (ERK) signaling plays a fundamental role in promoting cortical gliogenesis and the generation of cortical glial progenitors. Additionally, SHH-SMO-GLI activator signaling has an auxiliary function to ERK during these processes. We further demonstrate that NOTCH signaling is absolutely required for the fate determination of astrocytes, while ERK signaling plays a prominent role in oligodendrocyte fate specification, and SHH signaling is crucial for the fate determination of olfactory bulb interneurons from cortical progenitors. We provide evidence suggesting that this mechanism is conserved in both mice and humans. Finally, we propose a unifying principle of mammalian cortical gliogenesis.
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Project description:During cortical development, radial glial cells, known as neural stem cells, initially generate a large number of cortical glutamatergic pyramidal neurons through a process called neurogenesis. This is followed by the generation of a diversity of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, known as gliogenesis. However, the molecular mechanisms underlying the switch from cortical neurogenesis to gliogenesis, and the subsequent fate determination of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, remain unclear. Here, we report that extracellular signal-regulated kinase (ERK) signaling plays a fundamental role in promoting cortical gliogenesis and the generation of cortical glial progenitors. Additionally, SHH-SMO-GLI activator signaling has an auxiliary function to ERK during these processes. We further demonstrate that NOTCH signaling is absolutely required for the fate determination of astrocytes, while ERK signaling plays a prominent role in oligodendrocyte fate specification, and SHH signaling is crucial for the fate determination of olfactory bulb interneurons from cortical progenitors. We provide evidence suggesting that this mechanism is conserved in both mice and humans. Finally, we propose a unifying principle of mammalian cortical gliogenesis.
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Project description:Metabolic imbalance contributes to cognitive impairment, anxiety, depressive behavior, and impaired olfactory perception. As the synaptic signal from the olfactory bulb is directly transmitted to memory consolidation-related brain regions, recent studies have focused on the study of olfactory dysfunction in patients with obesity and diabetes accompanied by cognitive dysfunction. In this study, we investigated the transcriptomic change of olfactory bulb in high-fat diet-fed mice compared to that of normal diet-fed mice. We sampled olfactory bulbs from high fat diet mice, performed RNA sequencing, and measured protein and mRNA levels in olfactory bulb tissue. Also, we tested cytokine secretion in blood plasma of high fat diet mice. We found differences in the expression of protein-coding mRNAs and non-coding RNAs involved in insulin, lipid metabolism, neurogenesis, serotonin, dopamine, and gamma-aminobutyric acid-related signaling in the olfactory bulb of high-fat diet-fed mice compared to control mice. Our analyses suggest diverse targets for the treatment of olfactory dysfunction related to various neuropathologies in patients with metabolic syndrome.
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Project description:The olfactory system is a part of the mammalian central nervous system and is characterized by neurogenesis and replacement of degenerated neurons. Clinically, it has been reported that the various causes including aging, smoking, and epithelial damage have a high incidence of olfactory impairment. However, the molecular mechanisms underlying these causes-associated defect of olfaction have yet been unclear. To elucidate this problem, we performed micoarray analysis against mouse nasal mucosa and olfactory bulb and compared the transcriptome of them among groups.
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Project description:Gene expression profiling of mouse sclera during post-natal development
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Project description:To quantify gene expression differences in olfactory epithelium between the mouse (Mus musculus) and the Nile rat (Arvicanthis niloticus), paired-end RNA sequencing (RNA-seq) was used to profile olfactory epithelium transcriptomes of six Nile rats and six mice (C57BL/6J) (one male and one female at the age of 8, 12, and 16 weeks for each species).
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