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Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Xenopus laevis

PROVIDER: GSE115225 | GEO | 2019/01/16

REPOSITORIES: GEO

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Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [ChIP-seq]

Project description:VEGFA signaling is crucial for physiological and pathological angiogenesis and hematopoiesis. Although many context-dependent signaling pathways downstream of VegfA have been uncovered, vegfa transcriptional regulation in vivo is unclear. Here, we show that ETS transcription factor Etv6 positively regulates vegfa expression during blood stem cell development through multiple transcriptional inputs. In agreement with its established repressive functions, Etv6 directly inhibits expression of vegfa repressor foxo3. Surprisingly, it also directly activates expression of vegfa activator klf4. Finally, it indirectly binds to vegfa promoter by the recruiment of Klf4. Thus, our work uncovers a dual function for Etv6, as both a transcriptional repressor and activator, in controlling a major signaling pathway.

2019-01-16 | GSE115224 | GEO

Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [RNA-seq]

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Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo

Project description:Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo

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Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [RNA-seq]

Project description:Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [RNA-seq]

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Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [ChIP-seq]

Project description:Etv6-dependent positive and negative gene regulatory network controls vegfa expression in vivo [ChIP-seq]

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Etv6 activates vegfa expression through positive and negative transcriptional regulatory networks in Xenopus embryos.

Project description:VEGFA signaling controls physiological and pathological angiogenesis and hematopoiesis. Although many context-dependent signaling pathways downstream of VEGFA have been uncovered, vegfa transcriptional regulation in vivo remains unclear. Here, we show that the ETS transcription factor, Etv6, positively regulates vegfa expression during Xenopus blood stem cell development through multiple transcriptional inputs. In agreement with its established repressive functions, Etv6 directly inhibits expression of the repressor foxo3, to prevent Foxo3 from binding to and repressing the vegfa promoter. Etv6 also directly activates expression of the activator klf4; reflecting a genome-wide paucity in ETS-binding motifs in Etv6 genomic targets, Klf4 then recruits Etv6 to the vegfa promoter to activate its expression. These two mechanisms (double negative gate and feed-forward loop) are classic features of gene regulatory networks specifying cell fates. Thus, Etv6's dual function, as a transcriptional repressor and activator, controls a major signaling pathway involved in endothelial and blood development in vivo.

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FcR? controls the fas-dependent regulatory function of lymphoproliferative double negative T cells.

Project description:Patients with autoimmune lymphoproliferative syndrome (ALPS) and lymphoproliferation (LPR) mice are deficient in Fas, and accumulate large numbers of ??-TCR(+), CD4(-), CD8(-) double negative (DN) T cells. The function of these DN T cells remains largely unknown. The common ? subunit of the activating Fc receptors, FcR?, plays an important role in mediating innate immune responses. We have shown previously that a significant proportion of DN T cells express FcR?, and that this molecule is required for TCR transgenic DN T cells to suppress allogeneic immune responses. Whether FcR? plays a critical role in LPR DN T cell-mediated suppression of immune responses to auto and allo-antigens is not known. Here, we demonstrated that FcR?(+), but not FcR?(-) LPR DN T cells could suppress Fas(+) CD4(+) and CD8(+) T cell proliferation in vitro and attenuated CD4(+) T cell-mediated graft-versus host disease. Although FcR? expression did not allow LPR DN T cells to inhibit the expansion of Fas-deficient cells within the LPR context, adoptive transfer of FcR?(+), but not FcR?(-), DN T cells inhibited lymphoproliferation in generalized lymphoproliferative disease (GLD) mice. Furthermore, FcR? acted in a cell-intrinsic fashion to limit DN T cell accumulation by increasing the rate of apoptosis in proliferated cells. These results indicate that FcR? can confer Fas-dependent regulatory properties on LPR DN T cells, and suggest that FcR? may be a novel marker for functional DN Tregs.

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Hob6 positive and negative cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-16 | E-GEOD-45193 | biostudies-arrayexpress

A Grhl2-dependent gene network controls trophoblast branching morphogenesis

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

2015-03-10 | GSE65963 | GEO

Investigation of lncRNA-mRNA co-expression network in ETV6-RUNX1-positive pediatric B-cell acute lymphoblastic leukemia.

Project description:ETV6/RUNX1 gene fusion is the most common chromosomal translocation abnormality occurred in pediatric B-cell acute lymphoblastic leukemia (B-ALL). Compared with ETV6-RUNX1-negative patients, ETV6-RUNX1-positive patients possess more improved treatment strategies but higher risk to relapse. In this research, the potential gene interaction networks were constructed intending for elucidating the pathogenesis of B-ALL. We performed the weighted gene co-expression network analysis (WGCNA) to assess the involvement of lncRNA-mRNA pairs in B-ALL patients consisting of 24 ETV6-RUNX1-positive patients and 18 ETV6-RUNX1-negative patients and found a module that was significantly associated with positive/negative trait. Gene Ontology analysis showed that mRNAs in this module were enriched in the positive regulation of MAPK cascade, positive regulation of JNK cascade, and myeloid cell differentiation pathway. To further investigate the relationship between lncRNAs and mRNAs in this significant module, we constructed the lncRNA-mRNA co-expression network. 3 lncRNAs (RP11-170J3.2, RP11-135F9.1 and RP1-151B14.9) were found at the core of the lncRNA-mRNA co-expression network, which had the most co-expression connections with mRNAs. And several related mRNAs (ACTN1, TNFRSF21 and NLRP3) had a significant correlation with the patient survival prediction. Our findings may explicate the pathogenesis of B-ALL, and the disease-associated genes could provide clues to find novel biomarkers for prognosis.

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