Expression data from CD43- B220+ splenocytic B cells of WT and Cd37-/- C57BL/6J mice.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE212032 | GEO | 2022/08/26
REPOSITORIES: GEO
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Project description:Expression data from CD43- B220+ splenocytic B cells of WT and Cd37-/- C57BL/6J mice.
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Project description:The classic piebald mutation in the endothelin receptor type B (Ednrb) gene was found on rolling Nagoya genetic background (PROD-s/s) mice with white coat spotting. To examine whether genetic background influenced the phenotype in the piebald mutant mice, we generated a congenic strain (B6.PROD-s/s), produced by repeated backcrosses to the C57BL/6J (B6) strain. Although B6.PROD-s/s mice showed white coat spotting, 7% of B6.PROD-s/s mice died between 2 and 5 weeks after birth due to megacolon. The PROD-s/s, s/s and Japanese fancy mouse 1 (JF1) strains, which also have piebald mutations on different genetic backgrounds with B6, showed only pigmentation defects without megacolon. In expression analyses, rectums of B6.PROD-s/s with megacolon mice showed ~5% of the level of Ednrb gene expression versus B6 mice. In histological analyses, aganglionosis was detected in the rectum of megacolon animals. The aganglionic rectum was thought to lead to severe constipation and intestinal blockage, resulting in megacolon. We also observed an abnormal intestinal flora, including a marked increase in Bacteroidaceae and Erysipelotrichaceae and a marked decrease in Lactobacillus and Clostridiales, likely inducing endotoxin production and a failure of the mucosal barrier system, leading ultimately to death. These results indicate that the genetic background plays a key role in the development of enteric ganglion neurons, controlled by the Ednrb gene, and that B6 has modifier gene (s) regarding aganglionosis.
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Project description:To test the cell-specific function of GPR30 in learning and memory, we generated global GPR30 knockout (KO) mice (Δ3102), astrocyte-specific GPR30 KO (AG-KO) mice and neuron-specific GPR30 KO (NG-KO) mice. We found that GPR30 in astrocytes but not neurons is required to maintain normal learning and memory. To further elucidate the signaling pathway by which GPR30 plays a role in astrocyte function, high-throughput RNA sequencing of hippocampal tissues from Δ3102, AG-KO, and NG-KO mice was performed.
2023-08-10 | GSE212893 | GEO
Project description:Gene expression profiles in CIC KO CD4+ T cells
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Project description:Identification of genes in Smad3 WT and KO mice kidney
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Project description:Transcriptome analysis of skeletal muscle in large Maf KO mice
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Project description:The neuropeptide arginine vasopressin (AVP) plays significant roles in maintaining homeostasis and regulating social behavior. In vaginally delivered neonates, a surge of AVP is released into the bloodstream at levels exceeding release during life-threatening conditions such as hemorrhagic shock. It is currently unknown where the potential sites of action are in the neonate for these robust levels of circulating AVP at birth. The purpose of this study is to identify the location of AVP receptor 1a (AVPR1A) sites as potential peripheral targets of AVP in the neonatal mouse. RT-qPCR analysis of a sampling of tissues from the head demonstrated the presence of Avpr1a mRNA, suggesting local peripheral translation. Using competitive autoradiography in wildtype (WT) and AVPR1A knockout (KO) postnatal day 0 (P0) male and female mice on a C57BL/6J background, specific AVPR1A ligand binding was observed in the neonatal mouse periphery in sensory tissues of the head (eyes, ears, various oronasal regions), bone, spinal cord, adrenal cortex, and the uro-anogenital region in the neonatal AVPR1A WT mouse, as it was significantly reduced or absent in the control samples (AVPR1A KO and competition). AVPR1A throughout the neonatal periphery suggest roles for AVP in modulating peripheral physiology and development of the neonate.
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Project description:BackgroundTranscripts can exhibit significant variation in tissue samples from inbred laboratory mice. We have designed and carried out a microarray experiment to examine transcript variation across samples from adipose, heart, kidney, and liver tissues of C57BL/6J mice and to partition variation into within-mouse and between-mouse components. Within-mouse variance captures variation due to heterogeneity of gene expression within tissues, RNA-extraction, and array processing. Between-mouse variance reflects differences in transcript abundance between genetically identical mice.ResultsThe nature and extent of transcript variation differs across tissues. Adipose has the largest total variance and the largest within-mouse variance. Liver has the smallest total variance, but it has the most between-mouse variance. Genes with high variability can be classified into groups with correlated patterns of expression that are enriched for specific biological functions. Variation between mice is associated with circadian rhythm, growth hormone signaling, immune response, androgen regulation, lipid metabolism, and the extracellular matrix. Genes showing correlated patterns of within-mouse variation are also associated with biological functions that largely reflect heterogeneity of cell types within tissues.ConclusionsGenetically identical mice can experience different individual outcomes for medically important traits. Variation in gene expression observed between genetically identical mice can identify functional classes of genes that are likely to vary in the absence of experimental perturbations, can inform experimental design decisions, and provides a baseline for the interpretation of gene expression data in interventional studies. The extent of transcript variation among genetically identical mice underscores the importance of stochastic and micro-environmental factors and their phenotypic consequences.
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Project description:Tarsal joint abnormalities have been observed in aged male mice on a C57BL background. This joint disease consists of calcaneal displacement, inflammation, and proliferation of cartilage and connective tissue, that can progress to ankylosis of the joint. While tarsal pathology has been described previously in C57BL/6N substrains, as well as in STR/ort and B10.BR strain, no current literature describes this disease occurring in C57BL/6J mice. More importantly the behavioral features that may result from such a change to the joint have yet to be evaluated. This condition was observed in older male mice of the C57BL/6J lineage, around the age of 20 weeks or older, at a frequency of 1% of the population. To assess potential phenotypic sequela, this study sought to evaluate body weight, frailty assessment, home cage wheel running, dynamic weight bearing, and mechanical allodynia with and without the presence of pain relief with morphine. Overall mice with tarsal injuries had significantly higher frailty scores (p< 0.05) and weighed less (p<0.01) compared to unaffected mice. Affected mice had greater overall touch sensitivity (p<0.05) and they placed more weight on their forelimbs (p<0.01) compared to their hind limbs. Lastly, when housed with a running wheel, affected mice ran for a shorter length of time (p<0.01) but tended to run a greater distance within the time they did run (p<0.01) compared to unaffected mice. When tested just after being given morphine, the affected mice performed more similarly to unaffected mice, suggesting there is a pain sensation to this disease process. This highlights the importance of further characterizing inbred mouse mutations, as they may impact research programs or specific study goals.
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