Transcription profiling of curly tail mouse embryo
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Nicholas Greene
PROVIDER: E-MEXP-3673 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:We report single cell gene expression data for caudal tail tissue cells collected from embryos at 72 hours post fertilization (hpf).
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Project description:Using genome-wide transcriptional profiling and whole-mount expression analyses of zebrafish larvae, we have identified hyaluronan synthase 3 (has3) as an upregulated gene during caudal fin regeneration. has3 expression is induced in the wound epithelium within hours after tail amputation, and its onset and maintenance requires fibroblast growth factor, phosphoinositide 3-kinase, and transforming growth factor-β signaling. Inhibition of hyaluronic acid (HA) synthesis by the small molecule 4-methylumbelliferone (4-MU) impaired tail regeneration in zebrafish larvae by preventing injury-induced cell proliferation. In addition, 4-MU reduced the expression of genes associated with wound epithelium and blastema function. Treatment with the glycogen synthase 3-kinase inhibitors rescued 4-MU-induced defects in cell proliferation and tail regeneration, even though only a subset of wound epithelium and blastema markers was restored. Our findings uncover a role for HA biosynthesis in zebrafish tail regeneration and its epistatic relationships with other regenerative processes.
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Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomenon we examined the transcriptional response of the motor neurons after spinal cord injury. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurons 21 and 60 days after complete spinal transection where the tail exhibits clear signs of spasticity.
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Project description:We report transcriptional heterogeneity of venous endothelial cells (ECs) in the tail of zebrafish embryos, which consist of HSPC-niche-constituting ECs and caudal vessel (CV)-constituting ECs. To characterize isl1-derived ECs which derive from the endoderm and mainly constitute the HSPC niche in the caudal hematopoietic tissue (CHT), we performed single cell RNA sequencing (scRNA-seq) of isl1-derived ECs and the other ECs separately isolated from the tails of zebrafish embryos. Our analyses revealed that tail venous ECs were split into 5 distinct sub-clusters where isl1-derived ECs and the other ECs were similarly distributed to all venous EC clusters, and further revealed that genes whose expression levels are different between isl1-derived ECs and the other ECs tend to show similar changes across all of the clusters even after their diversification.
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Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomenon we examined the transcriptional response of the motor neurons after spinal cord injury. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurons 21 and 60 days after complete spinal transection where the tail exhibits clear signs of spasticity. Tail MNs were retorgradely labelled with flourogold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snab frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons were laser dissected into a collector tube to a total of ca. 50-200 cells pr sample. RNA was then extracted, two round amplified and hybridized to Affymetrix rat 230 2.0 arays. 27 samples were hybridized onto chips, 8 Spi-21, 8 Spi-60, 6 ShamC-21 and 5 ShamC-60.
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Project description:Tail amputation by tail docking or as an extreme consequence of tail biting in commercial pig production has serious implications for animal welfare. Tail amputation causes peripheral nerve injury that might be associated with chronic lasting pain. The aim of this study was to investigate the short- and long-term effects of tail amputation in pigs on caudal DRG gene expression at different stages of development, particularly in relation to genes associated with nociception and pain. Microarray analysis was used to analyse whole DRG transcriptomes from tail amputated and sham-treated pigs 1, 8 and 16 weeks following tail treatment at either 3 or 63 days of age (8 pigs/treatment/age/time after treatment; n=96). Tail amputation induced marked changes in gene expression (up and down) compared to sham-treated intact controls for all treatment ages and time points after tail treatment. Sustained changes in gene expression in tail amputated pigs were still evident approximately 4 months after tail injury. Gene correlation network analysis revealed two gene coexpression clusters associated with amputation. Gene ontology (GO) enrichment analysis found the genes in Cluster A (124 genes) and Cluster B (61 genes) to be associated with both ‘inflammatory pain’ and ‘neuropathic pain ’. Key families of ion channels and receptors were significantly down-regulated compared to shams in Cluster A, in particular voltage-gated potassium channels and GABA receptors which are both linked to increased peripheral nerve excitability after axotomy. Up-regulated functional gene families in Cluster B were linked to transcription regulation, inflammation, tissue remodelling and regulatory neuropeptide activity. DRG gene expression profiles appear to reflect sustained tissue inflammation and repair (ca. 4 months) and pain signal modulation consistent with adaptive, compensatory responses linked to injury induced increases in peripheral somatosensory neuronal excitability in the tail stump. Tail amputation causes acute and sustained changes in peripheral somatosensory nerve function involving key mediators of inflammatory and neuropathic pain which have implications for long-term tail stump pain. The findings of this study may have ramifications for the effects of tail amputation in other species. We used microarray to investigate the effects of tail amputation on gene expression in the dorsal root ganglia of caudal nerves in pigs at 2 treatment ages and 3 time points after tail treatment
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Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalizaion. To understand the moleclar mechanism behind this pheneomona we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after comlete spinal transection.
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Project description:IAP is one of the most transpositinally active retrotransposons in the mouse. Its transcription starts from the 5' long terminal repeat (LTR), and the expression level varied between cell types. This variation is thought to arise from differences in the epigenetic states, such as DNA methylation, of some copies of the 5' LTR between the cells. However, due to the high copy number and high sequence similarity, it was difficult to comprehensively and individually analyze epigenetic state of the IAP LTRs. Here, we developed a method called TEPBAT (Target Enrichment after Post-Bisulfite Adaptor Tagging) to analyze DNA methylation of individual retrotransposon copies. Using the method, we determined DNA methylation levels of >8,500 copies of genomic IAP LTRs (>97% of the copies targeted by the PCR primer) in sperm and tail. This revealed that the vast majority of the LTRs were heavily methylated both in sperm and tail, but hypomethylated copies were more frequently found in sperm than in tail. Interestingly, most of these hypomethylated LTRs were solo-type, belonged to specific subfamilies, and carried binding sites for transcription factors (TFs) active in male germ cells. We discuss possible roles for these TF-binding sites and the IAP internal sequence in regulation of LTR methylation.
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