publication_authors:Mercer EM Results

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Microarray (460)

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Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (383)

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Illumina Genome Analyzer IIx (23)

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Includes Publication (39)

GSE27402

Expression data from WT, HEB-KO and E2A-KO LY6D- CLP cells

Mus musculus
8 Downloadable Samples

Description

The E-protein transcription factors E2A and HEB play important roles at several stages of hematopoiesis. However, the exact mechanism for theire action and the main targets in the LY6D negative common lymphoid progentior (CLP) compartment remains unknown. By adressing this question, we will gain important infromation regarding the early events leading to B-cell specification.

Publication Title

The transcription factors E2A and HEB act in concert to induce the expression of FOXO1 in the common lymphoid progenitor.

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GSE30859

Multilineage Priming of Enhancer Repertoires Precedes Commitment to the B and Myeloid Cell Lineages in Hematopoietic Progenitors

Mus musculus
6 Downloadable Samples

Description

Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A (Tcf3) in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are premarked by the poised or active enhancer mark H3K4me1 in multipotent progenitors. Thus, in hematopoietic progenitors, multilineage priming of enhancer elements precedes commitment to the lymphoid or myeloid cell lineages.

Publication Title

Multilineage priming of enhancer repertoires precedes commitment to the B and myeloid cell lineages in hematopoietic progenitors.

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Specimen part

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GSE30855

Establishment of Enhancer Repertoires that Orchestrate the Myeloid and Lymphoid Cell Fates (gene expression dataset 1)

Mus musculus
6 Downloadable Samples

Description

Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are pre-marked by H3K4me1 in multipotent progenitors. However, H3K4me1 levels at a subset of enhancers are elevated during developmental progression, resulting in evolving enhancer repertoires that we propose orchestrate the myeloid and B cell fates.

Publication Title

Multilineage priming of enhancer repertoires precedes commitment to the B and myeloid cell lineages in hematopoietic progenitors.

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Specimen part

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GSE17840

Hedgehog is an anti-inflammatory epithelial signal for the intestinal lamina propria

Mus musculus
7 Downloadable Samples

Description

Epithelial Hedgehog (Hh) ligands regulate several aspects of fetal intestinal organogenesis and emerging data implicate the Hh pathway in inflammatory signaling in adult colon. We investigated the effects of chronic Hh inhibition in vivo and profiled molecular pathways acutely modulated by Hh signaling in the intestinal mesenchyme.

Publication Title

Hedgehog is an anti-inflammatory epithelial signal for the intestinal lamina propria.

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Specimen part

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GSE11723

Role of Notch signaling on hematopoietic stem cell differentiation

Mus musculus
9 Downloadable Samples

Description

Although Notch signaling has been clearly implicated in lymphoid differentiation, its role in myeloid lineages differentiation is unclear.

Publication Title

Notch signaling specifies megakaryocyte development from hematopoietic stem cells.

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SRP111553

Comparison of the expression profile of GFP-positive cells from Tg(-6.8wt1a:EGFP) with the rest of the cells in adult zebrafish cardiac ventricles

Danio rerio
16 Downloadable Samples
IlluminaHiSeq2500

Description

wt1a:GFP labels a population of subepicardial cells in the uninjured ventricle. Here we compare the expression profile of wt1a:GFP-positive cells to the rest of the cells of the ventricle. Overall design: Four paired biological replicates of wt1a:GFP-positive and wt1a:GFP-negative cells obtained from pools of 3-5 zebrafish heart ventricles.

Publication Title

Transient fibrosis resolves via fibroblast inactivation in the regenerating zebrafish heart.

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SRP062067

Telomerase is essential for zebrafish heart regeneration

Danio rerio
23 Downloadable Samples
IlluminaGenomeAnalyzerIIx

Description

Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction. Overall design: Heart transcriptomes of WT and telomerase defective adult zebrafish animals were profiled by RNASeq, in control conditions and 3 days after heart cryoinjury.

Publication Title

Telomerase Is Essential for Zebrafish Heart Regeneration.

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GSE21842

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells

Mus musculus
6 Downloadable Samples

Description

We report a Jak2V617F knock-in mouse myeloproliferative neoplasm (MPN) model resembling human polycythemia vera (PV). The MPN is serially transplantable and we demonstrate that the hematopoietic stem cell (HSC) compartment has the unique capacity for disease initiation but does not have a selective competitive advantage over wild type HSCs. In contrast, myeloid progenitor populations are expanded and skewed towards the erythroid lineage, but cannot transplant the disease. Treatment with a JAK2 kinase inhibitor ameliorated the MPN phenotype, but did not eliminate the disease-initiating population. These findings provide insights into the consequences of JAK2 activation on HSC differentiation and function and have the potential to inform therapeutic approaches to JAK2V617F positive MPN.