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Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells

ABSTRACT: Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells

PROVIDER: PRJNA510964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8359500_1.fastq.gz	Fastqsanger.gz
	SRR8359500_2.fastq.gz	Fastqsanger.gz
	SRR8359501_1.fastq.gz	Fastqsanger.gz
	SRR8359501_2.fastq.gz	Fastqsanger.gz
	SRR8359372.fastq.gz	Fastqsanger.gz

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Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (RNA-seq)

Project description:Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (RNA-seq)

| PRJNA510966 | ENA

Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (ChIP-seq)

Project description:Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (ChIP-seq)

| PRJNA510965 | ENA

Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (RNA-seq)

Project description:In this experiment, the differential gene expression was examined in intestinal epithelial cells of Mtg16 null mice compared to wild type.

2020-06-17 | GSE124185 | GEO

Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells (ChIP-seq)

Project description:In this experiment we analyse Mtg16 binding to chromatin in isolated mouse intestinal crypts from VillinCreER, Rbpjfl/fl mice 4 days following TM induction (Notch inhibition).

2020-06-17 | GSE124184 | GEO

Co-repressors Mtg8 and Mtg16 regulate niche exit and early fate decision of crypt stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-17 | GSE124186 | GEO

Kaiso is required for MTG16-dependent effects on colitis-associated carcinoma

Project description:The myeloid translocation gene family member MTG16 is a transcriptional corepressor that relies on the DNA-binding ability of other proteins to determine specificity. One such protein is the ZBTB family member Kaiso, and the MTG16:Kaiso interaction is necessary for repression of Kaiso target genes such as matrix metalloproteinase-7. Using the azoxymethane and dextran sodium sulfate (AOM/DSS) murine model of colitis-associated carcinoma, we previously determined that MTG16 loss accelerates tumorigenesis and inflammation. However, it was unknown whether this effect was modified by Kaiso-dependent transcriptional repression. To test for a genetic interaction between MTG16 and Kaiso in inflammatory carcinogenesis, we subjected single and double knockout (DKO) mice to the AOM/DSS protocol. Mtg16-/- mice demonstrated increased colitis and tumor burden; in contrast, disease severity in Kaiso-/- mice was equivalent to wild type controls. Surprisingly, Kaiso deficiency in the context of MTG16 loss reversed injury and pro-tumorigenic responses in the intestinal epithelium following AOM/DSS treatment, and tumor numbers were returned to near to wild type levels. Transcriptomic analysis of non-tumor colon tissue demonstrated that changes induced by MTG16 loss were widely mitigated by concurrent Kaiso loss, and DKO mice demonstrated downregulation of metabolism and cytokine-associated gene sets with concurrent activation of DNA damage checkpoint pathways as compared with Mtg16-/-. Further, Kaiso knockdown in intestinal enteroids reduced stem- and WNT-associated phenotypes, thus abrogating the induction of these pathways observed in Mtg16-/- samples. Together, these data suggest that Kaiso modifies MTG16-driven inflammation and tumorigenesis and suggests that Kaiso deregulation contributes to MTG16-dependent colitis and CAC phenotypes.

2019-04-02 | GSE124544 | GEO

MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors

Project description:Aberrant epithelial differentiation and regeneration contribute to colon pathologies, including inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Myeloid translocation gene 16 (MTG16, also known as CBFA2T3) is a transcriptional corepressor expressed in the colonic epithelium. MTG16 deficiency in mice exacerbates colitis and increases tumor burden in CAC, though the underlying mechanisms remain unclear. Here, we identified MTG16 as a central mediator of epithelial differentiation, promoting goblet and restraining enteroendocrine cell development in homeostasis and enabling regeneration following dextran sulfate sodium–induced (DSS-induced) colitis. Transcriptomic analyses implicated increased Ephrussi box–binding transcription factor (E protein) activity in MTG16-deficient colon crypts. Using a mouse model homozygous for a point mutation that attenuates MTG16:E protein interactions (Mtg16P209T), we showed that MTG16 exerts control over colonic epithelial differentiation and regeneration by repressing E protein–mediated transcription. Mimicking murine colitis, MTG16 expression was increased in biopsies from patients with active IBD compared with unaffected controls. Finally, uncoupling MTG16:E protein interactions partially phenocopied the enhanced tumorigenicity of Mtg16-null colon in the azoxymethane (AOM) /DSS-induced model of CAC, indicating that MTG16 protects from tumorigenesis through additional mechanisms. Collectively, our results demonstrate that MTG16, via its repression of E protein targets, is a key regulator of cell fate decisions during colon homeostasis, colitis, and cancer.

2022-05-01 | GSE201768 | GEO

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (ChIP-seq)

Project description:E protein transcription factors specify major immune cell lineages including lymphocytes and interferon-producing plasmacytoid dendritic cells (pDCs). Corepressors of the ETO family can bind to and block transactivation by E proteins, but the physiological role of these interactions remained unclear. We report that ETO protein Mtg16 binds chromatin primarily through the pDC-specific E protein E2-2 in human pDCs. Mtg16-deficient mice showed impaired pDC development and functionality, whereas the specification of the classical dendritic cells (cDCs) was enhanced. The deletion of Mtg16 caused aberrant expression of E protein antagonist Id2 in pDCs. Thus, Mtg16 acts as a cofactor of E2-2 to promote pDC differentiation and restrict cDC development, revealing an unexpected positive role of ETO proteins in E protein activity. Analysis of E2-2 and Mtg16 immunoprecipitated chromatin from CAL-1 cell line.

2014-06-13 | E-GEOD-43876 | biostudies-arrayexpress

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (gene expression)

Project description:E protein transcription factors specify major immune cell lineages including lymphocytes and interferon-producing plasmacytoid dendritic cells (pDCs). Corepressors of the ETO family can bind to and block transactivation by E proteins, but the physiological role of these interactions remained unclear. We report that ETO protein Mtg16 binds chromatin primarily through the pDC-specific E protein E2-2 in human pDCs. Mtg16-deficient mice showed impaired pDC development and functionality, whereas the specification of the classical dendritic cells (cDCs) was enhanced. The deletion of Mtg16 caused aberrant expression of E protein antagonist Id2 in pDCs. Thus, Mtg16 acts as a cofactor of E2-2 to promote pDC differentiation and restrict cDC development, revealing an unexpected positive role of ETO proteins in E protein activity. pDC from BM of WT and mtg16-KO mice were negatively selected (lin-CD19, Tcrb, Ter119, NK1.1) and sorted as CD11c+Bst2+ population directly in Trizol. RNA was prepared and deposited for microarray processing.

2014-06-13 | E-GEOD-43874 | biostudies-arrayexpress

Mtg16 regulates E protein activity and lineage specification in dendritic cell development (ChIP-seq)

2014-06-13 | GSE43876 | GEO