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RNA sequencing comparing the effect of the introduction of RUNX1-D171N in Csf3r-d715 mice bone marrow cells

ABSTRACT: RNA sequencing comparing the effect of the introduction of RUNX1-D171N in Csf3r-d715 mice bone marrow cells

PROVIDER: PRJEB39450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4352080_1.fastq.gz	Fastqsanger.gz
	ERR4352080_2.fastq.gz	Fastqsanger.gz
	ERR4352075_1.fastq.gz	Fastqsanger.gz
	ERR4352075_2.fastq.gz	Fastqsanger.gz
	ERR4352076_1.fastq.gz	Fastqsanger.gz

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RNA sequencing comparing the effect of the introduction of RUNX1-D171N in Csf3r-d715 mice bone marrow cells

Project description:To address how Csf3r and RUNX1 mutations in combination with CSF3 administration affect hematopoiesis in vitro, we performed hematopoietic expansion cultures in LODISH stem cell expansion medium. Lineage-negative Csfr-d715 BM cell cells were retrovirally transduced with the patient specific RUNX1-D171N (RHD) mutant or an empty vector control and subsequently treated with puromycin to select for the transduced cells. Lineage- c-Kit+ (LK) cells were FACS sorted in TRIzol 2, 5 and 9 days after puromycin selection and subsequently used for RNA isolation according to the manufacturer’s protocol. SMARTer Ultra Low Input RNA kit for sequencing (Clontech, v4 Cat# 634891) was used to generate cDNA. Sequencing libraries were generated using TruSeq Nano DNA Sample Preparation kits (Illumina, Cat# 20015964), according to the low sample protocol and paired-end sequenced on a HiSeq 2500 (Illumina).

2020-08-24 | E-MTAB-9373 | biostudies-arrayexpress

RNA sequencing comparing the effect of the introduction of RUNX1-D171N (RHD) in control- or SCN -CSF3R-d715 hematopoietic progenitor cells (HPCs)

Project description:To address how CSF3R and RUNX1 mutations affect hematopoiesis in a severe congenital neutropenia (SCN) background we used SCN patient, or control, derived induced pluripotent stem cells (iPSC). HPCs were generated from CRISPR-Cas9 genome edited CSF3R-d715 SCN or control-derived iPSCs with the STEMdiff™ Hematopoietic Kit (STEMCELL Technologies). The RUNX1-D171N (RHD) mutation, or an empty vector control, was lentivirally introduced to the hematopoietic induction cultures 60 hours before harvesting the floating cells. Floating cells were harvested at Day 12 of the hematopoietic induction protocol. CD34+CD45+ HPCs were FACS sorted in TRIzol and RNA was isolated according to the manufacturer’s protocol. SMARTer Ultra Low Input RNA kit for sequencing (Clontech, v4 Cat# 634891) was used to generate cDNA. Sequencing libraries were generated using TruSeq Nano DNA Sample Preparation kits (Illumina, Cat# 20015964), according to the low sample protocol and paired-end sequenced on a HiSeq 2500 or Novaseq 6000 (both Illumina).

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RUNX1-ETO translocations must proceed CSF3R mutations to promote acute myeloid leukemia development

Project description:Acute myeloid leukemia (AML) is a deadly blood cancer character by an overproduction of immature myeloid cells. AML has a high degree of genetic diversity, and the presence or absence of particular genetic alterations can greatly impact prognosis. In AML, patients with CSF3R mutations exhibit high relapse rates and poor overall survival. A recent study found that 90.5% of patients with CSF3R mutations had cooccurring RUNX1-ETO (8;21), CBFB-MYH11, or CEBPA mutations7. The RUNX1-ETO and CBFB-MYH11 translocations disrupt the core binding factor complex, an important transcriptional regulator in myeloid development. In this study, we evaluated how RUNX1-ETO modifies CSF3RT618I-driven transcriptional changes to promote the production of myeloblasts in AML. We find that RUNX1-ETO accelerates CSF3R-driven oncogenesis both in vitro and in vivo. Furthermore, RUNX1-ETO impairs the ability of CSF3R to drive myeloid differentiation associated transcriptional programs resulting in the production of immature myeloblasts which characterize this disease.

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CSF3R T618I collaborates with RUNX1-RUNX1T1 to expand hematopoietic progenitors and sensitizes to GLI-inhibition [single-cell RNA-seq]

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Project description:Effects of TET2 on repressing inflammation have been assigned to its methylcytosine dioxygenase activity, but also to its ability to recruit HDAC-mediated repressor activity to pro-inflammatory genes. To discriminate between the two above-proposed functions of TET2, we asked how inhibition of its enzymatic activity, by administration of octyl-(R)-2hydroxyglutarate (2HG), and its ability to recruit HDAC-activity, by administration of the HDAC-inhibitor MS275 (Entinostat), affected the transcriptional profile of CSF3R-d715 RUNX1-D171N (RHD) expressing SCN-iPSC derived CD34+CD45+ HPCs. HPCs were generated from CRISPR-Cas9 genome edited CSF3R-d715 SCN-derived iPSCs with the STEMdiff™ Hematopoietic Kit (STEMCELL Technologies). The RUNX1-D171N (RHD) mutation was lentivirally introduced to the hematopoietic induction cultures 60 hours before harvesting the floating cells. DMSO (solvent control), 0.1 mM Octyl-(R)-2HG (Sigma-Aldrich) or 2 µM MS275 (Santa Cruz) was added for 16 hours to the hematopoietic induction cultures before harvesting the floating cells. Floating cells were harvested at Day 12 of the hematopoietic induction protocol. CD34+CD45+ HPCs were FACS sorted in TRIzol and RNA was isolated according to the manufacturer’s protocol. SMARTer Ultra Low Input RNA kit for sequencing (Clontech, v4 Cat# 634891) was used to generate cDNA. Sequencing libraries were generated using TruSeq Nano DNA Sample Preparation kits (Illumina, Cat# 20015964), according to the low sample protocol and paired-end sequenced on a Novaseq 6000 (Illumina).

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CSF3R T618I collaborates with RUNX1-RUNX1T1 to expand hematopoietic progenitors and sensitizes to GLI-inhibition

Project description:CSF3R T618I collaborates with RUNX1-RUNX1T1 to expand hematopoietic progenitors and sensitizes to GLI-inhibition

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