Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA178664 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR610740_1.fastq.gz | Fastqsanger.gz | |||
| SRR610740_2.fastq.gz | Fastqsanger.gz | |||
| SRR610741_1.fastq.gz | Fastqsanger.gz | |||
| SRR610741_2.fastq.gz | Fastqsanger.gz | |||
| SRR610742_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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Project description:Human oncogenes involved in the development of hematological malignancies have been widely used to model experimental leukemia. Here, we used the fli1 promoter in zebrafish to target the expression of oncogenic HRAS to endothelial cells, including the hemogenic endothelium and observed the development of a myelo-erythroid proliferative disease. In larvae, the pathological phenotype is characterized by some disruption of the vascular system with prominent expansion of the caudal hematopoietic tissue, increase of expression of stem cell markers and myelo-erythroid specific genes and production of a large number of l-plastin leukocytes. In mosaic juveniles, increased number of hematopoietic blasts and arrest of myeloid maturation was found in kidney marrow. Peripheral blood showed delays of erythrocyte maturation and increased number of circulating myeloid progenitors. We found that the abnormal phenotype is associated with a down regulation of the Notch pathway as shown by the decrease of expression of Notch target genes, whereas overexpressing an activated form of Notch together with the oncogene prevents the expansion of the myelo-erythroid compartment. This study identifies the downregulation of the Notch pathway following an oncogenic event in the hemogenic endothelium as an important step in the pathogenesis of myelo-erythroid diseases and describes a number of potential effectors of this transformation. Methods: mRNA profiles of transgenic zebrafish overexpressing the oncogene HRAS in endothelial cells (Tg(fli1ep:GAL4FF)ubs3; Tg(UAS:eGFP-HRASV12)io006); or expressing activate Notch in endothelial cells (Tg(fli1ep:GAL4FF)ubs3; tg(UAS:NICD)kca3) were generated by deep sequencing using Illumina HiSeq 2000. The sequence reads that passed quality filters were analyzed using the CLC bio Assembly Cell software (version 3.2) and the Ensembl (release 63) predicted cDNAs for the Zv9 genome assembly. qRTM-bM-^@M-^SPCR validation was performed using TaqMan and SYBR Green assays.
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Project description:Human oncogenes involved in the development of hematological malignancies have been widely used to model experimental leukemia. Here, we used the fli1 promoter in zebrafish to target the expression of oncogenic HRAS to endothelial cells, including the hemogenic endothelium and observed the development of a myelo-erythroid proliferative disease. In larvae, the pathological phenotype is characterized by some disruption of the vascular system with prominent expansion of the caudal hematopoietic tissue, increase of expression of stem cell markers and myelo-erythroid specific genes and production of a large number of l-plastin leukocytes. In mosaic juveniles, increased number of hematopoietic blasts and arrest of myeloid maturation was found in kidney marrow. Peripheral blood showed delays of erythrocyte maturation and increased number of circulating myeloid progenitors. We found that the abnormal phenotype is associated with a down regulation of the Notch pathway as shown by the decrease of expression of Notch target genes, whereas overexpressing an activated form of Notch together with the oncogene prevents the expansion of the myelo-erythroid compartment. This study identifies the downregulation of the Notch pathway following an oncogenic event in the hemogenic endothelium as an important step in the pathogenesis of myelo-erythroid diseases and describes a number of potential effectors of this transformation.
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Project description:Integration of index sorting and single cell functional assays allowed identification of novel haematopoietic stem cell (HSC) and multiprogenitor subsets (MPP) that differ in their lineage differentiation potential in vitro and in vivo, cell cycle properties and long-term repopulation capacity in the NSG xenograft model. Here we report single cell transcriptomes of CD49f+ HSCs as well as those of CD49f+ Subset1 (CD19- CD38- CD45RA- CD90+ CD49f+ CD34lo CLEC9Ahi, Myelo-erythroid-skewed in vitro but Lymphoid-competent) and CD49f+ Subset2 cells (CD19- CD38- CD45RA- CD90+ CD49f+ CD34hi CLEC9Alo, Myelo-Lymphoid competent but Erythroid-deficient). We also report bulk transcriptomes of pools of 20 cells from HSC/MPP Subset1 (CD19- CD38- CD45RA- CD34lo CLEC9Ahi) and HSC/MPP Subset2 (CD19- CD38- CD45RA- CD34hi CLEC9Alo). Altogether these data show a diffuse transcriptional landscape of the CD49f+ HSC compartment, which is polarised along an axis that separates Myelo-Erythroid and Myelo-Lymphoid lineage-priming. Consistently with their differentiation capacity in vitro, CD49f+ Subset1 cells cluster at the Myelo-Erythroid end of the landscape, while CD49f+ Subset2 cells cluster at the Myelo-Lymphoid end. In addtion, these lineage-priming signatures were found to be more marked in HSC/MPP Subset1 and HSC/MPP Subset2, than in the equivalent CD49f+ subsets. In conclusion, 49f+ Subset1 and 49f+ Subset2 populations have activated distinct transcriptional lineage-priming programmes corresponding to the phenotypic lineage-skewing observed in vitro, that then become reinforced within the broader HSC/MPP pool. Altogether our data shows that lineage-priming and lineage-restriction programmes are initially established within the CD49f+ HSC subset in humans.
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