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Role of Hopx in myogenesis and commitment [ChIP-Seq]

ABSTRACT: Hopx is expressed in cardiomyoblasts, progenitors commited to the myocyte fate. ChIP-seq experiements were performed to understand Hopx occupancy in E9.5 hearts. An epitope tagged allele, in which a 3X-Flag sequence is appeneded to the endogenous Hopx transcript. Our results suggest that Hopx occupancy is enriched in regions close to Wnt family members, confirmed by gene ontology analysis and indepedent expression analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE67251 | GEO | 2015/06/01

SECONDARY ACCESSION(S): PRJNA279347

REPOSITORIES: GEO

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Role of Hopx in myogenesis and commitment [HopxKO]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from 1. Hopx +/- embryoid bodies, 2. Hopx -/- embryoid bodies, Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67253 | GEO

Role of Hopx in myogenesis and commitment [HopxKO+Wnt]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from Hopx +/- embryoid bodies or Hopx -/- embryoid bodies treated with 12.5 uM XAV939. Heterozygous embryoid bodies included 0 uM XAV939, a well-characterized, known Wnt inhibitor. Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67252 | GEO

Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

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Next generation sequencing for quantitative transcriptomic analysis of Hopx-wildtype and Hopx-knockout murine bone marrow cells.

Project description:We generated Hopx conditional knockout mouse (Hopx-/-) and studied the biological effects of Hopx knockout on the hematopoietic system, via whole-transcriptome RNA-seq. The findigns of our studies support crucial roles of Hopx in physiological and malignant hematopoiesis.

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Next generation sequencing for quantitative transcriptomic analysis of subpopulations of BM cells from young Hopx-wildtype and Hopx-knockout mice.

Project description:Hopx conditional knockout mouse (Hopx-/-) was generated. We then studied the biological effects of Hopx knockout on the hematopoietic system of young mice, via whole-transcriptome RNA-seq.

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Competitive regulation of HOPX transcription governs cardiomyocyte maturation

Project description:This study establishes the homeodomain only protein, HOPX, as a determinant controlling the molecular switch between cardiomyocyte progenitor and maturation gene programs. This dataset is about time-course CAGE (capped analysis of gene expression) data with genome-wide active transcription footprinting. HOPX CRISPRi cells were differentiated into cardiomyocytes ± DOX and analyzed by CAGE sequencing, among other methods. The study revealed that HOPX interacts with and controls core cardiac networks by regulating the activity of mutually exclusive developmental gene programs.

2022-05-21 | E-MTAB-11719 | biostudies-arrayexpress

HOP homeobox (Hopx) and Histone deacetylase-2 (Hdac2) deficiency effect on the embryonic heart

Project description:Analysis of heart ventricles from Hopx, Hdac2, and both Hopx-Hdac2 deficient embryos at embryonic day E16.5. Results provide insight into the role of Hopx and Hdac2 in cardiac development. We used microarrays to detail the global programme of gene expression underlying cardiac development by Hopx and Hdac2 and identified distinct classes of up-regulated and down-regulated genes during this process. Mouse embryonic ventricles were selected at E16.5 for RNA extraction and hybridization on Affymetrix microarrays. We obtained three independent embryonic ventricles for WT, Hopx-null, Hdac2-null, and Hopx-Hdac2 double null genotypes.

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Plasticity of Hopx+ Type I alveolar cells to regenerate Type II cells in the lung

Project description:Hopx is a transcription co-factor expressed during lung development and we wanted to profile Hopx +/+ and -/- embyonic lungs. Results inform the role of Hopx in embryonic lung development We used microarrays to profile the transcriptome of Hopx -/- lungs compared to Hopx +/+ lungs. Lungs were microdissected and three biological replicates were used for each genotype.

2015-02-10 | E-GEOD-65755 | biostudies-arrayexpress

Homeodomain-only protein (HOPX) negatively regulates CD8+ T cell proliferation and affects differentiation and aging

Project description:HOPX is an atypical homeodomain-containing protein lacking DNA-binding capacity. Via interaction with transcription factors, particularly SRF, it has critical functions in the development of various tissues. Here we unveil an essential regulatory role of HOPX in human T lymphocytes. Human CD8+ T cells expressed all three isoforms (a, b, and c) of HOPX wherein HOPXb was the predominant one. HOPX expression was induced by TCR activation and increased from TN to TEM cells. Overexpression of HOPX constrained the proliferation of TN cells while knockdown of HOPX promoted the proliferation of TEM cells upon TCR activation. Mechanistically, HOPX/SRF bound to the promoters and repressed expression of MYC and NR4A1, the key regulators of T cell proliferation and activation. Importantly, CD8+ T cells from the elderly had elevated levels of HOPX, correlated with their blunted TCR-induced proliferation. Knockdown of HOPX rescued the proliferative capacity of T cells from the elderly. Our results support that HOPX is a molecular switch that balances CD8+ T cell proliferation across subsets and with age.

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