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Single-cell RNA sequencing revealed the transcriptional landscape and heterogeneity of macrophages in the intestinal tissues of WT and RUNX3 macrophage conditional knockout mice.

ABSTRACT: Single-cell RNA sequencing revealed the transcriptional landscape and heterogeneity of macrophages in the intestinal tissues of WT and RUNX3 macrophage conditional knockout mice.

PROVIDER: PRJNA1215379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32117600_1.fastq.gz	Fastqsanger.gz
	SRR32117600_2.fastq.gz	Fastqsanger.gz
	SRR32117593_1.fastq.gz	Fastqsanger.gz
	SRR32117593_2.fastq.gz	Fastqsanger.gz
	SRR32117594_1.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing revealed the transcriptional landscape and heterogeneity of macrophages in the intestinal tissues of WT and RUNX3 macrophage conditional knockout mice.

Project description:CD11b+ cell populations, especially macrophages, are highly heterogeneous tissue-resident immune cells in mice and humans. The exact subpopulation and its phenotype remain unknown. Here, we analyzed intestinal CD11b+ cell populations from normal and Runx3 macrophage conditionally deficient mice using scRNA-seq. We found that the transcription factor RUNX3 plays a key role in the entry of inflammatory monocytes into resident macrophages. Decreased resident macrophages and elevated ZFP36 in RUNX3flow/flowlyz2-Cre mice, leading to cytokine and chemokine degradation in colon tissue-resident macrophages. RUNX3 promotes the expression of NR4A1, thereby inducing the differentiation of inflammatory monocytes into resident macrophages. Single-cell population analysis revealed that the ERK1/2/MAPK pathway plays a key role in NR4A1-mediated gut-resident macrophage differentiation.

2025-01-29 | GSE287970 | GEO

The affect of specific ablation of Runx3 from Esam splenic dendritic cells

Project description:Esam/CD4+ dendritic cells are part of the innate immunity essential for priming and activating of CD4+ T cells To identify Runx3 responsive genes Esam dendritic cells were freshly sorted from macs enriched splenic DCs taken from 6 weeks old mice. Four samples from four mice were sorted and analyzed where in each littermates pair consisted of a control and Runx3 conditional KO. Mice lacking Runx3 specifically in the DC compartment were produced by crossing Runx3fl/fl mice onto CD11c-Cre mice. This mating scheme generated Runx3fl/fl/CD11c:Cre (CD11c-DC-Runx3Δ) mice.

2014-06-22 | E-GEOD-48590 | biostudies-arrayexpress

Runx3 function in colon resident macrophages (RM) and CD11b+ dendritic cells (DC).

Project description:RUNX3 is one of three mammalian Runt-domain transcription factors that regulate gene expression in several types of immune cells. Runx3-deficiency in mice is associated with a multitude of defects in the adaptive and innate immunity systems, including the development of early onset colitis. Our study reveals that conditional deletion of Runx3 specifically in mononuclear phagocytes (MNP) recapitulates the early onset spontaneous colitis seen in Runx3-/- mice. We show that Runx3 is expressed in colonic MNP, including RM and the dendritic cell cDC2 subsets and its loss results in impaired differentiation/maturation of both cell types. To uncover the immuno-tolerogenic properties of Runx3 in the colon MNP we performed global transcriptional profiling employing microarrays.

2020-06-04 | GSE136066 | GEO

The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

2019-11-12 | PXD007511 | Pride

Transcriptome analysis of MAZR and/or Runx3-deficient cytotoxic T lymphocytes

Project description:We investigated transcriptional changes in MAZR-, Runx3- and MAZR/Runx3-deficient cytotoxic T lymphocytes (CTLs). This analysis revealed that MAZR plays a compensatory role in the Runx3-dependent transcriptional program of CTL differentiation.

2021-03-11 | GSE129772 | GEO

RNA-seq of E11.5 TrkC neurons of Runx3-P2+/- and Runx3-P2-/- mice

Project description:To gain insight into the role of Runx3 in TrkC neurons we performed RNA-seq on E11.5 TrkC neurons isolated from cervical ganglia of Runx3-P2+/- and Runx3-P2-/- mice

2016-11-20 | GSE81140 | GEO

RUNX3 Facilitates Growth of Ewing Sarcoma Cells

Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA

2014-05-01 | E-GEOD-56900 | biostudies-arrayexpress

Runx3 function in splenic NK cells

Project description:NK cells are innate immune cells that recognize and kill foreign, virally-infected and tumor cells without the need for prior immunization. NK expansion following viral infection is IL-2 or IL-15-dependent. To identify Runx3 responsive genes, NK cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of freshly isolated NK cells (resting) were separately obtained from individual mice.

2013-11-18 | E-GEOD-50123 | biostudies-arrayexpress

Genome wide map of Runx3 bound regions in murine splenic CD8 T cells

Project description:Runx3 is an important transcription factor for the proper development of CD8+T cells. The number and functionality of CD8+T cells is severely affected in the absence of Runx3. To gain insight into the transcriptional program managed by Runx3 in CD8+T cells we conducted ChIP-seq on 50 million cells and CUT&RUN on 150,000 cells, using anti Runx3 antibodies. Both assays revealed similar results.

2021-01-12 | GSE164536 | GEO

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (HiChIP)

Project description:Gastric cancer metastasis is a major cause of mortality worldwide. Inhibition of RUNX3 in gastric cancer cell lines reduced migration, invasion, and anchorage independent growth in vitro. Following splenic inoculation, CRISPR-mediated RUNX3-knockout HGC-27 cells show suppression of xenograft growth and liver metastasis. We interrogated the potential of RUNX3 as a metastasis driver in gastric cancer by profiling its target genes. Transcriptomic analysis revealed strong involvement of RUNX3 in the regulation of multiple developmental pathways, consistent with the notion that RUNX family genes are master regulators of development. RUNX3 promoted “cell migration” and “extracellular matrix” programs, which are necessary for metastasis. Of note, we found pro-metastatic genes WNT5A, CD44 and VIM among the top differentially expressed genes in RUNX3-knockout versus control cells. Chromatin immunoprecipitation sequencing and HiChIP analyses revealed that RUNX3 bound to the enhancers and promoters of these genes, suggesting that they are under direct transcriptional control by RUNX3. We show that RUNX3 promoted metastasis in part through its upregulation of WNT5A to promote migration, invasion, and anchorage-independent growth in various malignancies. Our study therefore reveals the RUNX3-WNT5A axis as a key targetable mechanism for gastric cancer metastasis.

2023-12-20 | GSE250480 | GEO

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