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Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic cell lines co-occupied with lineage specific regulators (GATA1, GATA2, CEBPA)

ABSTRACT: Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration. This represents the human ChIP-seq portion of this dataset on leukemia cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29195 | GEO | 2011/10/07

SECONDARY ACCESSION(S): PRJNA142955

REPOSITORIES: GEO

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Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic cell lines co-occupied with lineage specific regulators (GATA1, GATA2, CEBPA)

Project description:Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration. This represents the human ChIP-seq portion of this dataset on leukemia cell lines. Human hematopoietic cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total Smad1 (Santa Cruz SC-7965), Tcf7l2 (Santa Cruz SC-8631),Gata1 (Santa Cruz SC-265), Gata2 (Santa Cruz SC-9008), CEBPA (SC-9314) or H3K4me1 (Abcam ab8895).

2011-10-07 | E-GEOD-29195 | biostudies-arrayexpress

Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic progenitors co-occupied with lineage specific regulators (GATA1, GATA2)

2011-10-07 | GSE29194 | GEO

Genome-wide location analysis of WNT (Tcf7l2) and BMP (SMAD1) in human hematopoeitic progenitors co-occupied with lineage specific regulators (GATA1, GATA2)

Project description:Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration. This represents the human CD34 ChIP-seq portion of this dataset. Human hematopoietic cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total Smad1 (Santa Cruz SC-7965), Tcf7l2 (Santa Cruz SC-8631),Gata1 (Santa Cruz SC-265), Gata2 (Santa Cruz SC-9008) or CEBPA (SC-9314).

2011-10-07 | E-GEOD-29194 | biostudies-arrayexpress

Genome-wide location analysis of BMP (SMAD1) in mouse erythroid progenitors co-occupted with lineage specific regulators (GATA1, GATA2)

Project description:Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration Mouse G1E or G1ER cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total Smad1 (Santa Cruz SC-7965), Gata1 (Santa Cruz SC-265), or Gata2 (Santa Cruz SC-9008). This represents the Mouse ChIP-seq portion of this dataset.

2011-10-07 | E-GEOD-29193 | biostudies-arrayexpress

Genome-wide location analysis of BMP (SMAD1) in mouse erythroid progenitors co-occupted with lineage specific regulators (GATA1, GATA2)

Project description:Lineage regulators direct BMP and Wnt pathways to cell-specific programs during differentiation and regeneration

2011-10-07 | GSE29193 | GEO

BMP-SMAD1/5 Signaling Regulates Retinal Vascular Development.

Project description:Vascular development is an orchestrated process of vessel formation from pre-existing vessels via sprouting and intussusceptive angiogenesis as well as vascular remodeling to generate the mature vasculature. Bone morphogenetic protein (BMP) signaling via intracellular SMAD1 and SMAD5 effectors regulates sprouting angiogenesis in the early mouse embryo, but its role in other processes of vascular development and in other vascular beds remains incompletely understood. Here, we investigate the function of SMAD1/5 during early postnatal retinal vascular development using inducible, endothelium-specific deletion of Smad1 and Smad5. We observe the formation of arterial-venous malformations in areas with high blood flow, and fewer and less functional tip cells at the angiogenic front. The vascular plexus region is remarkably hyperdense and this is associated with reduced vessel regression and aberrant vascular loop formation. Taken together, our results highlight important functions of SMAD1/5 during vessel formation and remodeling in the early postnatal retina.

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Project description:Recognition that germline mutations can predispose individuals to blood cancers, often presenting as secondary leukemias, has largely been driven in the last 20 years by studies of families with inherited mutations in the myeloid transcription factors (TFs) RUNX1, GATA2, and CEBPA. As a result, in 2016, classification of myeloid neoplasms with germline predisposition for each of these and other genes was added to the World Health Organization guidelines. The incidence of germline mutation carriers in the general population or in various clinically presenting patient groups remains poorly defined for reasons including that somatic mutations in these genes are common in blood cancers, and our ability to distinguish germline (inherited or de novo) and somatic mutations is often limited by the laboratory analyses. Knowledge of the regulation of these TFs and their mutant alleles, their interaction with other genes and proteins and the environment, and how these alter the clinical presentation of patients and their leukemias is also incomplete. Outstanding questions that remain for patients with these germline mutations or their treating clinicians include: What is the natural course of the disease? What other symptoms may I develop and when? Can you predict them? Can I prevent them? and What is the best treatment? The resolution of many of the remaining clinical and biological questions and effective evidence-based treatment of patients with these inherited mutations will depend on worldwide partnerships among patients, clinicians, diagnosticians, and researchers to aggregate sufficient longitudinal clinical and laboratory data and integrate these data with model systems.

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Allele-specific expression of GATA2 due to epigenetic dysregulation in CEBPA double-mutant AML.

Project description:Transcriptional deregulation is a central event in the development of acute myeloid leukemia (AML). To identify potential disturbances in gene regulation, we conducted an unbiased screen of allele-specific expression (ASE) in 209 AML cases. The gene encoding GATA binding protein 2 (GATA2) displayed ASE more often than any other myeloid- or cancer-related gene. GATA2 ASE was strongly associated with CEBPA double mutations (DMs), with 95% of cases presenting GATA2 ASE. In CEBPA DM AML with GATA2 mutations, the mutated allele was preferentially expressed. We found that GATA2 ASE was a somatic event lost in complete remission, supporting the notion that it plays a role in CEBPA DM AML. Acquisition of GATA2 ASE involved silencing of 1 allele via promoter methylation and concurrent overactivation of the other allele, thereby preserving expression levels. Notably, promoter methylation was also lost in remission along with GATA2 ASE. In summary, we propose that GATA2 ASE is acquired by epigenetic mechanisms and is a prerequisite for the development of AML with CEBPA DMs. This finding constitutes a novel example of an epigenetic hit cooperating with a genetic hit in the pathogenesis of AML.

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SMAD1 and SMAD5 Expression Is Coordinately Regulated by FLI1 and GATA2 during Endothelial Development.

Project description:The bone morphogenetic protein (BMP)/SMAD signaling pathway is a critical regulator of angiogenic sprouting and is involved in vascular development in the embryo. SMAD1 and SMAD5, the core mediators of BMP signaling, are vital for this activity, yet little is known about their transcriptional regulation in endothelial cells. Here, we have integrated multispecies sequence conservation, tissue-specific chromatin, in vitro reporter assay, and in vivo transgenic data to identify and validate Smad1+63 and the Smad5 promoter as tissue-specific cis-regulatory elements that are active in the developing endothelium. The activity of these elements in the endothelium was dependent on highly conserved ETS, GATA, and E-box motifs, and chromatin immunoprecipitation showed high levels of enrichment of FLI1, GATA2, and SCL at these sites in endothelial cell lines and E11 dorsal aortas in vivo. Knockdown of FLI1 and GATA2 but not SCL reduced the expression of SMAD1 and SMAD5 in endothelial cells in vitro. In contrast, CD31(+) cKit(-) endothelial cells harvested from embryonic day 9 (E9) aorta-gonad-mesonephros (AGM) regions of GATA2 null embryos showed reduced Smad1 but not Smad5 transcript levels. This is suggestive of a degree of in vivo selection where, in the case of reduced SMAD1 levels, endothelial cells with more robust SMAD5 expression have a selective advantage.

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Tbx1 regulates the BMP-Smad1 pathway in a transcription independent manner.

Project description:Tbx1 is a T-box transcription factor implicated in DiGeorge syndrome. The molecular function of Tbx1 is unclear although it can transactivate reporters with T-box binding elements. We discovered that Tbx1 binds Smad1 and suppresses the Bmp4/Smad1 signaling. Tbx1 interferes with Smad1 to Smad4 binding, and a mutation of Tbx1 that abolishes transactivation, does not affect Smad1 binding nor does affect the ability to suppress Smad1 activity. In addition, a disease-associated mutation of TBX1 that does not prevent transactivation, prevents the TBX1-SMAD1 interaction. Expression of Tbx1 in transgenic mice generates phenotypes similar to those associated with loss of a Bmp receptor. One phenotype could be rescued by transgenic Smad1 expression. Our data indicate that Tbx1 interferes with Bmp/Smad1 signaling and provide strong evidence that a T-box transcription factor has functions unrelated to transactivation.

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