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Differential analysis of HOXA1 in adult cells at isoform resolution by RNA-Seq [Illumina]

ABSTRACT: High-throughput RNA sequencing (RNA-Seq) has enabled accurate gene discovery and expression estimation, but robust differential analysis of gene and transcript abundances has proven difficult. We present a new algorithm, implemented in the freely available tool Cuffdiff, which integrates transcript-level expression estimation with a method to control for variability across replicate samples. Cuffdiff robustly identifies differentially regulated isoforms and genes and reveals differential splicing or promoter-preference changes. We demonstrate the accuracy of our approach through differential analysis of lung fibroblasts in response to loss of the developmental transcription factor HOXA1 and uncover a critical role for this gene in the maintenance of adult cells. We show that HOXA1 is required for lung fibroblast and HeLa cell cycle progression, and loss of HOXA1 results in significant expression level changes in thousands of individual transcripts, along with isoform switching events in key regulators of the cell cycle.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37703 | GEO | 2012/12/11

SECONDARY ACCESSION(S): PRJNA162905

REPOSITORIES: GEO

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Differential analysis of HOXA1 in adult cells at isoform resolution by RNA-Seq [Agilent]

Project description:High-throughput RNA sequencing (RNA-Seq) has enabled accurate gene discovery and expression estimation, but robust differential analysis of gene and transcript abundances has proven difficult. We present a new algorithm, implemented in the freely available tool Cuffdiff, which integrates transcript-level expression estimation with a method to control for variability across replicate samples. Cuffdiff robustly identifies differentially regulated isoforms and genes and reveals differential splicing or promoter-preference changes. We demonstrate the accuracy of our approach through differential analysis of lung fibroblasts in response to loss of the developmental transcription factor HOXA1 and uncover a critical role for this gene in the maintenance of adult cells. We show that HOXA1 is required for lung fibroblast and HeLa cell cycle progression, and loss of HOXA1 results in significant expression level changes in thousands of individual transcripts, along with isoform switching events in key regulators of the cell cycle.

2012-12-11 | GSE37690 | GEO

Differential analysis of HOXA1 in adult cells at isoform resolution by RNA-Seq [Illumina]

2012-12-11 | E-GEOD-37703 | biostudies-arrayexpress

Differential analysis of HOXA1 in adult cells at isoform resolution by RNA-Seq [Agilent]

2012-12-11 | E-GEOD-37690 | biostudies-arrayexpress

Identification of Hoxa1 downstream targets

Project description:To better understand the role of Hoxa1 during embryogenesis and gain insight to the transcriptional network controlled by this gene, we carried out a large-scale screening for Hoxa1 downstream targets by performing microarray analysis. Tissue from the rhombomere 3-5 region of wildtype and Hoxa1 null embryos, including neuroectoderm, mesoderm and otic ectoderm was microdissected at the peak of Hoxa1 expression. RNA from wildtype and Hoxa1Δ/Δ samples was hybridized to the Agilent mouse whole genome array.

2011-09-03 | GSE25868 | GEO

Modeling myelodysplastic syndromes in mice by altered Hoxa1 spliceform expression

Project description:The homeobox gene, Hoxa1, has two different isoforms generated by alternative splicing: a full-length homeodomain-containing Hoxa1 (Hoxa1-FL), and a truncated Hoxa1 (Hoxa1-T), that lacks the homeodomain. Oncoretroviral overexpression of wildtype Hoxa1 cDNA (WT-Hoxa1), which generates both Hoxa1 isoforms, in murine hematopoietic stem and progenitor cells (HSPCs) perturbed hematopoiesis, resulting in myelodysplastic syndromes (MDS) in mice. Overexpression of a mutated Hoxa1 cDNA (MUT-Hoxa1) that generates Hoxa1-FL but not Hoxa1-T led to a more severe MDS capable of transforming to secondary acute myeloid leukemia (sAML). Similar to human MDS, DNA damage repair pathways were downregulated in Hoxa1-overexpressing hematopoietic progenitor cells. Conditional knock-in mouse models revealed a Hoxa1-FL dosage-dependent effect on MDS disease severity. Our data reveal that increased expression of Hoxa1-FL in HSPCs is sufficient to initiate MDS in mice. CD34+ cells from up to 50% of patients with MDS had elevated HOXA1-FL expression, highlighting the clinical relevance of our mouse models.

2023-11-28 | GSE62853 | GEO

Modeling myelodysplastic syndromes in mice by altered Hoxa1 spliceform expression (CMP)

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Hoxa1 LoF RNA-seq

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Identification of Hoxa1 downstream targets

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Project description:Hoxa1 LoF RNA-seq

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A distal enhancer maintaining Hoxa1 expression orchestrates retinoic acid-induced early ESCs differentiation

Project description:Retinoic acid (RA) induces rapid differentiation of ESCs, partly by activating expression of the transcription factor Hoxa1, which regulates downstream target genes that promote ESCs differentiation. However, mechanisms of RA-induced Hoxa1 expression and ESCs early differentiation remain largely unknown. Here, we identify a distal enhancer interacting with the Hoxa1 locus through a long-range chromatin loop. Enhancer deletion significantly inhibited expression of RA-induced Hoxa1 and endoderm master control genes such as Gata4 and Gata6. Transcriptome analysis revealed that RA-induced early ESCs differentiation was blocked in Hoxa1 enhancer knockout cells, suggesting a requirement for the enhancer. Restoration of Hoxa1 expression partly rescued expression levels of ~40% of genes whose expression changed following enhancer deletion, and ~18% of promoters of those rescued genes were directly bound by Hoxa1. Our data show that a distal enhancer maintains Hoxa1 expression through long-range chromatin loop and that Hoxa1 directly regulates downstream target gene expression and then orchestrates RA-induced early differentiation of ESCs.

2018-12-24 | GSE124306 | GEO

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