Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176457 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transcription factor Egr3 has been shown to have a cell autonomous role in sympathetic nervous system (SNS) development. We utilized microarray analysis to identify potential downstream target genes deregulated with loss of Egr3. Both conditions were in the null Bax background to prevent apoptosis and therefore mitigate identification of apoptosis related genes. Our analysis identified genes involved in biological processes that were expected such as SNS development and axonogenesis as well as those that were unexpected such as dendritogenesis and axon guidance. This led us to investigate whether Egr3 is important in these unexpected biological processes within sympathetic neurons. Total RNA was obtained from superior cervical ganglion (SCG) dissected from P0 mice with the genotype of Egr3+/+; Bax-/- or Egr3-/-; Bax-/-. Each genotype had 3 samples each.
2013-03-22 | E-GEOD-41290 | biostudies-arrayexpress
Project description:The transcription factor Egr3 has been shown to have a cell autonomous role in sympathetic nervous system (SNS) development. We utilized microarray analysis to identify potential downstream target genes deregulated with loss of Egr3. Both conditions were in the null Bax background to prevent apoptosis and therefore mitigate identification of apoptosis related genes. Our analysis identified genes involved in biological processes that were expected such as SNS development and axonogenesis as well as those that were unexpected such as dendritogenesis and axon guidance. This led us to investigate whether Egr3 is important in these unexpected biological processes within sympathetic neurons.
2013-03-22 | GSE41290 | GEO
Project description:Gene expression in groups of sympathetic neurons from an NPY reporter mouse
| PRJNA320420 | ENA
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:To uncover Meis1 functions during the embryonic development of sympathetic neurons, we perfomed a ChIP-seq analysis from mouse E16 embryonic superior cervical ganglia (SCG) using an antibody against Meis1. We identified 309 potential target genes with a particular enrichment in genes involved in vesicles formation, function and trafficking, leading to the hypothesis that Meis1 participate in late sympathetic neurons differentiation by coordinating target-field innervation, synaptogenesis and survival through the transcriptional control of the machinery necessary for endocytosis and exocytosis. We further confirmed that the expression of some of these genes was lost and/or modified in E16 SCGs of a HtPACRE/Meis1LoxP/LoxP mouse strain compared to wild type littermates. We additionaly confirmed that endocytosis and synaptogenesis is impaired in those mutants.
2015-09-30 | GSE54144 | GEO
Project description:Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared to controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism underlying the disturbance of diurnal rhythmicity in cardiac disease and suggest means for therapeutic intervention.
2023-07-20 | GSE231766 | GEO
Project description:Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared to controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism underlying the disturbance of diurnal rhythmicity in cardiac disease and suggest means for therapeutic intervention.
2023-07-20 | GSE233223 | GEO
Project description:Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared to controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism underlying the disturbance of diurnal rhythmicity in cardiac disease and suggest means for therapeutic intervention.
2023-07-20 | GSE231765 | GEO
Project description:Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared to controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism underlying the disturbance of diurnal rhythmicity in cardiac disease and suggest means for therapeutic intervention.
2023-07-20 | GSE231764 | GEO
Project description:Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared to controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism underlying the disturbance of diurnal rhythmicity in cardiac disease and suggest means for therapeutic intervention.
2023-07-20 | GSE231763 | GEO