Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA386262 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report genome-wide gene expression changes in olfactory bulb cells, in the context of low, wild-type or high levels of local CRH signaling by local interneurons onto adult-born CRHR1+ granule neurons. To test the gene expression changes associated with altered local CRH signaling, we utilize the following animal models: CRHR1-/- mice whose bulbs were infected with a control AAV-flex-EGFP virus = low local CRH signaling, CRHR1-Cre mice whose bulbs were infected with AAV-flex-EGFP = pseudo-wild-type local CRH signaling, and CRHR1-Cre mice whose bulbs were infected with AAV-flex-(CA)CRHR1, which is a constitutively active variant of CRHR1 = high local CRH signaling. We find that, in response to changes in local CRH signaling in the bulb, the largest ontological category of transcription changes in the bulb that occurs reciprocally between low and high levels of CRH signaling are gene regulatory factors. To test the contributions of one of these factors, POU6f1, we perform loss- and gain-of-function analysis. We show that CRHR1 activation results in transcriptional activation of POU6f1 and that POU6f1 in turn influences synaptogenesis and dendritic patterning of adult-born neurons and olfactory circuit behavior.
2017-10-26 | GSE98799 | GEO
Project description:A subset of COVID-19 patients exhibit altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium and olfactory bulb that express cell entry molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find that samples from whole olfactory mucosa in species including mouse and human express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, neither olfactory sensory neurons nor olfactory bulb neurons express these genes, which are instead expressed in support cells, stem cells, and perivascular cells. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.
2020-07-30 | GSE148360 | GEO
Project description:A subset of COVID-19 patients exhibit altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium and olfactory bulb that express cell entry molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find that samples from whole olfactory mucosa in species including mouse and human express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, neither olfactory sensory neurons nor olfactory bulb neurons express these genes, which are instead expressed in support cells, stem cells, and perivascular cells. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.
2020-07-30 | GSE151346 | GEO
Project description:Olfactory ensheathing cells (OECs) are neural crest-derived glia that ensheath bundles of olfactory axons from their peripheral origins in the olfactory epithelium to their central targets in the olfactory bulb. We took an unbiased laser microdissection and differential RNA-seq approach, validated by in situ hybridisation, to identify candidate molecular mechanisms underlying mouse OEC development and differences with the neural crest-derived Schwann cells developing on other peripheral nerves. We identified 25 novel markers for developing OECs in the olfactory mucosa and/or the olfactory nerve layer surrounding the olfactory bulb, of which 15 were OEC-specific, i.e., not expressed by Schwann cells. One pan-OEC-specific gene, Ptprz1, encodes a receptor-like tyrosine phosphatase that blocks oligodendrocyte differentiation. Mutant analysis suggests Ptprz1 may also act as a brake on OEC differentiation, and that its loss disrupts olfactory axon targeting. Overall, our results provide new insights into OEC development and the diversification of neural crest-derived glia.
2020-06-02 | GSE138596 | GEO
Project description:The goal of this study is to profile NFIA DNA-binding properties in the adult mouse brain. We performed chromatin immunoprecipitation of NFIA in the hippocampus and olfactory bulb of wildtype mice, and samples were subjected to sequencing. We find that NFIA preferentially binds DNA in the hippocampus but not in the olfactory bulb as evidenced by the distinct lack of NFIA binding peaks in the olfactory bulb. Mass spectrometry results suggested that NFIA has a significantly higher binding affinity for NFIB in the olfactory bulb, potentially blocking NFIA’s ability to bind DNA. Virally induced siRNAs against NFIB or scramble were injected into the olfactory bulb of adult wildtype mice to knock down NFIB. We performed chromatin immunoprecipitation of NFIA in the olfactory bulb injected with siRNA-NFIB or siRNA-scramble. Subsequent sequencing revealed an increase of NFIA binding in the olfactory bulb upon the depletion of NFIB as compared to the siRNA-scramble and wildtype controls.
2020-02-28 | GSE146064 | GEO
Project description:Proteome analysis of mouse brain tissue samples from olfactory bulb of middle-aged (8-13 months) female mice.
2020-09-16 | PXD017766 | Pride
Project description:The goals of this study are to profile the molecular signatures of astrocytes from four brain regions (olfactory bulb, hippocampus, cortex, and brainstem) and determine if differential transcription factor enrichment may play a role in shaping astrocyte spatial diversity. We performed RNA-seq on astrocytes from the olfactory bulb, hippocampus, cortex, and brainstem, and determined region-specific molecular signatures. Using transcription factor motif discovery analysis on each region-specific gene signature we uncovered universal and region-specific transcription factor expression profiles.
2020-01-13 | GSE143282 | GEO
Project description:There is an emerging concern that particulate air pollution increases the risk of cranial nerve disease onset. Small nanoparticles, mainly derived from diesel exhaust particles reach the olfactory bulb by their nasal depositions. It has been reported that diesel exhaust inhalation causes inflammation of the olfactory bulb and other brain regions. However, these toxicological studies have not evaluated animal rearing environment. We hypothesized that rearing environment can change mice phenotypes and thus might alter toxicological study results. In this study, we exposed mice to diesel exhaust inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days after rearing in a standard cage or environmental enrichment conditions. Microarray analysis found that expression levels of 112 genes were changed by diesel exhaust inhalation. Functional analysis using Gene Ontology revealed that the dysregulated genes were involved in inflammation and immune response. This result was supported by pathway analysis. Quantitative RT-PCR analysis confirmed 10 genes. Interestingly, background gene expression of the olfactory bulb of mice reared in a standard cage environment was changed by diesel exhaust inhalation, whereas there was no significant effect of diesel exhaust exposure on gene expression levels of mice reared with environmental enrichment. The results indicate for the first time that the effect of diesel exhaust exposure on gene expression of the olfactory bulb was influenced by rearing environment. Rearing environment, such as environmental enrichment, may be an important contributive factor to causation in evaluating still undefined toxic environmental substances such as diesel exhaust. RNA sample was taken from olfactory bulb of 56-day-old mouse received diesel exhaust (DE) inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days, while control RNA was taken from mouse received clean air, after rearing in a standard cage or environmental enrichment conditions. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
2013-04-18 | E-GEOD-46163 | biostudies-arrayexpress
Project description:Global gene expression profiling was performed using RNA from human embryonic neural stem cells (hENSCs) and adult human olfactory bulb-derived neural stem cells (OBNSCs) to define a gene expression pattern and signaling pathways that are specific for each cell lineage. Subtractive gene expression profiling between both cell lineages provides a list of potential genes that are related to their multipotentiality, proliferation, migration, and alternative signaling pathways. To confirm the validity of our DNA microarray data, our results were compared with data from various databases. The gene expression profile of adult olfactory bulb neural stem cells (n=6) was compared with that of human embryonic neural stem cells (n=3).
2012-01-30 | E-GEOD-35390 | biostudies-arrayexpress
Project description:During development of the nervous system, neurons connect to one another in a precisely organized manner. Sensory systems provide a good example of this organization, whereby the composition of the outside world is represented in the brain by neuronal maps. Establishing correct patterns of neural circuitry is crucial, as inaccurate map formation can lead to severe disruptions in sensory processing. In rodents, olfactory stimuli modulate a wide variety of behaviours essential for survival. The formation of the olfactory glomerular map is dependent on molecular cues that guide olfactory receptor neuron axons to broad regions of the olfactory bulb and on cell adhesion molecules that promote axonal sorting into specific synaptic units in this structure. Here, we demonstrate that the cell adhesion molecule Amigo1 is expressed in a subpopulation of olfactory receptor neurons, and we investigate its role in the precise targeting of olfactory receptor neuron axons to the olfactory bulb using a genetic loss-of-function approach in mice. While ablation of Amigo1 did not lead to alterations in olfactory sensory neuron axonal targeting, our experiments revealed that the presence of a neomycin resistance selection cassette in the Amigo1 locus can lead to off-target effects that are not due to loss of Amigo1 expression, including unexpected altered gene expression in olfactory receptor neurons and reduced size of glomeruli in the ventral region of the olfactory bulb. Our results demonstrate that insertion of a neomycin selection cassette into the mouse genome can have specific deleterious effects on the development of the olfactory system and highlight the importance of removing antibiotic resistance cassettes from genetic loss-of-function mouse models when studying olfactory system development.
2024-02-26 | GSE249314 | GEO