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HoxA3 is an apical regulator of hemogenic endothelium

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE25079: Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium GSE25080: Genes regulated by HoxA3 in endothelial and hematopoietic progenitors Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Michael Kyba

PROVIDER: E-GEOD-25096 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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HoxA3 is an apical regulator of haemogenic endothelium.

Iacovino Michelina M Chong Diana D Szatmari Istvan I Hartweck Lynn L Rux Danielle D Caprioli Arianna A Cleaver Ondine O Kyba Michael M

Nature cell biology 20101219 1

During development, haemogenesis occurs invariably at sites of vasculogenesis. Between embryonic day (E) 9.5 and E10.5 in mice, endothelial cells in the caudal part of the dorsal aorta generate haematopoietic stem cells and are referred to as haemogenic endothelium. The mechanisms by which haematopoiesis is restricted to this domain, and how the morphological transformation from endothelial to haematopoietic is controlled are unknown. We show here that HoxA3, a gene uniquely expressed in the emb ...[more]

PMID: 21170035

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Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium

Project description:We observe that HoxA3 represses hematopoieis by the repression of several transcription factors including Runx1 and Gata1. Up regulation of either Runx1 or Gata1 in the presence of HoxA3 reverted the hematopoietic repression. We have performed full genome analysis to determine the molecular signature of hematopoietic development in response to upregulation of Runx1 and Gata1. Endothelial progenitors were sorted from HoxA3 induced EBs, transduced with either control vector (control), Runx1 vector or Gata1 vector. Cells were co-cultured on Op9 for 5 days: in the following conditions: Control, HoxA3 upregulation, HoxA3 + Runx1 upregulation, HoxA3 + Gata1 upregulation in triplicate. After 5 days of culture,transduced cells were sorted (5000 cells) and prepared for microarray.

2010-12-20 | E-GEOD-25079 | biostudies-arrayexpress

Genes regulated by HoxA3 in endothelial and hematopoietic progenitors

Project description:We used a murine ES cell line in which HoxA3 expression is under control of a tetracycline-responsive element and differentiated these cells as embryoid bodies (EBs). Endothelial (Flk-1 VE-cadherin double positive, FV) and hematopoieitc progenitors (c-Kit CD41 double positive, K41) were isolated from differentiated EBs that had been induced for 6 hours by doxycycline (Dox) treatment. Here we show genes regulated upon HoxA3 upregulation (6 hours doxycycline treatment) in hematopoietic and endothelial progenitors.

2010-12-20 | E-GEOD-25080 | biostudies-arrayexpress

Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium

2010-12-20 | GSE25079 | GEO

HOXA3 expression in wound tissue

Project description:To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid. In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Disease State: cutaneous wound/control skin unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3

2009-10-12 | E-GEOD-13324 | biostudies-arrayexpress

HOXA3 expression in wound tissue

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Upregulation of HOXA3 by Isoform-Specific Wilms Tumor 1 Drives Chemotherapy Resistance in Acute Myeloid Leukemia

Project description:Upregulation of the Wilms' Tumor 1 (WT1) gene is common in acute myeloid leukemia (AML) and is associated with poor prognosis, including disease relapse, decreased overall survival (OS), and chemotherapy resistance. WT1 produces 12 primary transcripts through different translation initiation sites and alternative splicing, but the specific transcripts and mechanisms responsible for chemoresistance are unknown. We found that overexpression of short WT1 transcripts lacking exon 5 with and without the KTS motif (sWT1+/- and sWT1-/-) led to reduced cell growth. However, only sWT1+/- resulted in decreased CD71 expression, G1 arrest, and cytarabine resistance. Primary AML patient cells with low CD71 expression exhibit relative resistance to cytarabine, suggesting that CD71 may serve as a potential biomarker for cytarabine therapy. RNAseq differential gene expression analysis identified two transcription factors, HOXA3 and GATA2, that are specifically upregulated in sWT1+/- cells. Overexpression of either HOXA3 or GATA2 reproduced the effects of sWT1+/-, including decreased cell growth, G1 arrest, reduced CD71 expression, and cytarabine resistance. Furthermore, sWT1+/-, HOXA3, and GATA2 regulate cell growth and cytarabine sensitivity in a context-dependent manner, likely dependent on HOXA3 expression. HOXA3 expression is significantly correlated with chemotherapy response, OS, and ELN subtypes in NPM1-negative leukemia specimens. Overexpression of HOXA3 leads to drug resistance against a broad spectrum of chemotherapeutic agents. Our results suggest that WT1 modulates drug sensitivity in an isoform-specific manner by promoting HOXA3 expression. Both HOXA3 mRNA and CD71 cell surface expression could serve as potential biomarkers for predicting responses to cytarabine-based treatment in AML.

2024-07-31 | GSE239734 | GEO

ChIP-seq for Hoxa3 on mouse posterior branchial arches at E11.5.

Project description:Hoxa3 ChIP-seq on mouse posterior branchial arches connected to outflow tract of the heart (PBA/OFT) at embryonic day (E) 11.5.

2020-10-16 | E-MTAB-8607 | biostudies-arrayexpress

Genes regulated by HoxA3 in endothelial and hematopoietic progenitors

2010-12-20 | GSE25080 | GEO

Dual actions of Meis1 inhibit erythroid progenitor development and sustain general hematopoietic cell proliferation

Project description:This SuperSeries is composed of the following subset Series: GSE34537: Mesp1 induces a subset of hematopoietic-associated transcription factors in ES cell-derived Flk1+Tie2+ endothelium GSE34541: Identification of gene targets of Meis2 GSE34543: Identification of gene targets of Meis1 Refer to individual Series

2012-08-02 | E-GEOD-34583 | biostudies-arrayexpress

HOXA3 functions as the on-off switch to regulate the development of hESC-derived third pharyngeal pouch endoderm through EPHB2-mediated Wnt pathway

Project description:Normal commitment of the endoderm of the third pharyngeal pouch (3PP) is essential for the development and differentiation of the thymus. The aim of this study was to investigate the role of transcription factor HOXA3 in the development and differentiation of the third pharyngeal pouch endoderm from human embryonic stem cells (hESCs). 3PP endoderm (3PPE) was differentiated from hESC-derived definitive endoderm (DE) by mimicking developmental queues with Activin A, WNT3A, retinoic acid and BMP4. The function of 3PPE was assessed by further differentiating into functional thymic epithelial cells. The effect of HOXA3 inhibition on cells of 3PPE was subsequently investigated. A highly efficient approach for differentiating 3PPE cells has been developed and these cells expressed 3PPE related genes HOXA3, SIX1, PAX9 as well as EpCAM. 3PPE cells had a strong potential to develop into thymic epithelia which expressed both the cortical epithelial cell markers K8 and CD205, and the medullary epithelial cell markers K5 and AIRE, and also promoted T cell maturation. More importantly, transcription factor HOXA3 not only regulated the differentiation of 3PPE, but also had a crucial role for the proliferation and migration 3PPE cells. Our further investigation revealed that HOXA3 controlled the commitment and function of 3PPE through the regulation of the Wnt signaling pathway by EPHB2. Our results demonstrated that HOXA3 functioned as the on-off switch to regulate the development of hESC-derived 3PPE through EPHB2-mediated Wnt pathway, and our findings will provide new insights into studying the development of the third pharyngeal pouch and thymic organ in vitro and in vivo.

2023-07-24 | GSE237751 | GEO

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