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RNA-seq of long-term hematopoietic stem cells and myeloid progenitors of control mice or mice conditionally deficient for Trp53 or Elp3 or both genes in the hematopoietic system

ABSTRACT: RNA-seq of long-term hematopoietic stem cells and myeloid progenitors of control mice or mice conditionally deficient for Trp53 or Elp3 or both genes in the hematopoietic system

PROVIDER: PRJEB27627 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2683590_1.fastq.gz	Fastqsanger.gz
	ERR2683590_2.fastq.gz	Fastqsanger.gz
	ERR2683600_1.fastq.gz	Fastqsanger.gz
	ERR2683600_2.fastq.gz	Fastqsanger.gz
	ERR2683591_1.fastq.gz	Fastqsanger.gz

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RNA-seq of long-term hematopoietic stem cells and myeloid progenitors of control mice or mice conditionally deficient for Trp53 or Elp3 or both genes in the hematopoietic system

Project description:Aim of the experiment was to compare the gene expression responses of long-term hematopoietic stem cells (HSCs) and myeloid-restricted progenitors (MyPs) to the hematopoietic cell-restricted deletion of the catalytic subunit Elp3 of the Elongator complex. Since Elp3 deletion resulted in activation of the p53 pathway, we also studied the transcriptome of MyPs deficient for Trp53 or for both Elp3 and Trp53. The Elp3fl/fl strain was generated in house and first described in (DOI: 10.1084/jem.20142288). The Trp53 strain was first described in (DOI: 10.1101/gad.14.8.994) and was purchased from the Jackson Laboratory. Littermates of 8-12 weeks old were used in all experiments.

2020-12-10 | E-MTAB-6992 | biostudies-arrayexpress

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2020-12-10 | E-MTAB-9628 | biostudies-arrayexpress

Polysome profiling analysis of myeloid progenitors of control mice or mice conditionally deficient for Elp3 in the hematopoietic system

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NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

Project description:NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

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RNAseq of follicular helper T cell from Elp3 deficient mice after Complete Freund Adjuvant immunisation

Project description:Loss of Elp3 in CD4 T cells hindered the development of an optimal T follicular helper T cell (TFH) response. To understand the molecular pathway by which Elp3 is necessary for TFH responses, mice deficient for Elp3 in T cells and WT littermate were immunized with ovalbumin emulsified with complete Freund Adjuvant. 8 days later, TFH were sorted from the draining lymph nodes and submitted for RNAseq

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Single cell transcriptomic analysis of bone marrow hematopoietic stem and progenitors cells isolated from 10-week-old wild-type control, Rps19R67∆/R67∆, Rps19R67∆/R67∆ Trp53−/− and Trp53−/− mutant mice.

Project description:This single cell transcriptome sequencing experiment is part of the study \\"Preclinical animal model of Diamond-Blackfan anemia with single amino acid mutation of ribosomal protein Rps19\\". A mouse model with this mutation develops features characteristic of human Diamond-Blackfan anemia, a rare bone marrow failure syndrome, including hematologic dysfunctions, early onset growth delay, intrinsic anemia, severe craniofacial, skeletal, urogenital, cardiovascular, and cerebral abnormalities leading to premature lethality during the adolescence of the mouse. This DBA mouse model exhibits cell intrinsic activation of the Trp53 signaling pathway in hematopoietic stem cells (HSCs) leading to reduced erythroid lineage development that may be rescued after inactivation of the tumor suppressor Trp53. The study uncovers that the development of the DBA phenotype significantly involves non-canonical components of the p53 signaling pathway in the etiopathogenesis of DBA with the Rps19R67∆ mutation leading to the disrupted hematopoietic hierarchy starting at the stage of short-term repopulating stem cells and the central role of induced Trp53 expression and upregulation of its non-canonical targets in the mediation of neural crest lineage deficiency-mediated development of craniofacial malformations in this model.

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