RNA-Sequencing of Xenopus tail regeneration using small molecule antagonists of Hif1a or Wnt signaling
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ABSTRACT:
PROVIDER: PRJNA731541 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14608200_1.fastq.gz | Fastqsanger.gz | |||
| SRR14608200_2.fastq.gz | Fastqsanger.gz | |||
| SRR14608201_1.fastq.gz | Fastqsanger.gz | |||
| SRR14608201_2.fastq.gz | Fastqsanger.gz | |||
| SRR14608202_1.fastq.gz | Fastqsanger.gz |
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Project description:Regeneration of complex tissues is initiated by an injury-induced stress response, eventually leading to activation of developmental signaling pathways, such as Wnt signaling. How early injury cues are interpreted and coupled to activation of these developmental signals and their targets is not well understood. Here, we show that Hif1α, a stress induced transcription factor, is required for tail regeneration in Xenopus tropicalis. We find that Hif1α is required for regeneration of differentiated axial tissues, including axons and muscle. Using RNA-sequencing, we find that Hif1α and Wnt converge on a broad set of genes required for posterior specification and differentiation, including the posterior hox genes. We further show that Hif1α is required for transcription via a Wnt-responsive element, a function that is conserved in both regeneration and early neural patterning. Our findings indicate a regulatory role for Hif1α in Wnt mediated gene expression across multiple tissue contexts.
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2010-10-01 | E-MEXP-2420 | biostudies-arrayexpress
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Project description:Premetamorphic Xenopus laevis tadpole tail respond to thyroid hormone by resorption. The goal of this experiment is to identify the genes involved in the TH-induced resorption tadpole tail and compare it to TH-induced proliferation and differentiation program in tadpole limb and brain. Xenopus tadpoles (NF54) were treated with 100 nM T3 in 0.1 x MMR for another 24h and 48h or without T3 for 48h (control group). NF 61 tadpoles were in 0.1 X MMR till they reached NF stage 62. The tails were dissected after the experiment. Keywords: development or differentiation design,organism part comparison design,reference design,replicate design,time series design
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Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. Whereas, dragon fly also induced higher tail tadpole. The tadpoles revert to a normal phenotype upon removal of the larval salamander or dragon fly threat. The objective of the present study was to use Affymetrix Xenopus Genechip to profile gene expression in the tail tissue by different predation threat. Tadpoles of Rana pirica treated with larvae salamander for 8days (S1, S2, S3) or dragon fly for 8days (Y1,Y2, Y3) were analyzed with triplicate. Removal experiments were also treated with predators for 4days and then removed predators from tadpoles (-S1,-S2, -S3) or (-Y1,-Y2,-Y3). Controls were cultured for 8days without predators (C2, C3). Tails from tadpoles after 8days of each treatment were dissected for RNA extraction and gene expression analysis using Affymetrix Xenopus Genechip arrays.
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Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. Whereas, dragon fly also induced higher tail tadpole. The tadpoles revert to a normal phenotype upon removal of the larval salamander or dragon fly threat. The objective of the present study was to use Affymetrix Xenopus Genechip to profile gene expression in the tail tissue by different predation threat.
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Project description:Xenopus laevis tadpoles differ in their regenerative potential according to their developmental stage. Here, we focus on tail regeneration following amputation. By comparing the regenerative response during the naturally occurring regeneration-competent and -incompetent stages, scRNAseq can reveal cell type changes that are required for successful regeneration.
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Project description:The Mexican axolotl provides a powerful model to investigate mechanisms of tissue regeneration. A recent chemical screen found that HDAC inhibitor romidepsin, administered for only 1-minute post amputation (1 MPA), blocks axolotl tail regeneration. Here, we tested the potential for cobalt chloride (CoCl2), a chemical stabilizer of HIF1a and inducer of hypoxia, to rescue romidepsin-inhibition of tail regeneration. Tail regeneration was partially rescued when embryos with amputated tails were co-treated with romidepsin and CoCl2. However, extending the CoCl2 dosage window either inhibited regeneration (CoCl2:0-30 MPA) or was lethal (CoCl2:0-24 hours post amputation; HPA). CoCl2:0-30 MPA caused tissue damage, tissue loss, and cell death at the distal tail tip, and blocked regeneration. In contrast, CoCl2 treatment of non-amputated embryos or CoCl2:60-90 MPA treatment of amputated embryos did not affect wound healing or inhibit tail regeneration. To further investigate the contrasting effects of CoCl2, microarray analysis was performed to identify differentially expressed genes at 3 HPA. CoCl2-romidepsin:1 MPA treatment significantly increased the expression of transcription factors associated with appendage regeneration, while CoCl2:0-30 MPA significantly increased expression of hemoglobin and platelet-specific transcripts, consistent with hemorrhage and an impaired hemostatic response. Also, CoCl2:0-30 MPA significantly increased expression of hypoxia inducible genes, including genes that encode Hif1a interacting proteins and heat shock proteins (HSP); in contrast, genes encoding TGFB signaling components were significantly downregulated. Using additional chemical inhibitors of tail regeneration, we identified transcriptional responses associated with HSP90 activity and TGFB signaling. Notably, geldanamcin decreased transcription of matrix metalloproteinases and sustained muscle-specific gene expression, suggesting a role for HSP90 in regulating extracellular matrix remodeling and muscle dedifferentiation. Our study shows the power of using chemical tools to precisely identify temporal windows within which critical biological processes are enacted during tissue regeneration.
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