ArticleCell reports2015
The alternative splicing regulator Tra2b is required for somitogenesis and regulates splicing of an inhibitory Wnt11b isoform.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Splicing of ultraconserved poison exons controls mitotic fidelity and stem cell viability.bioRxiv : the preprint server for biology · 2026Article
- Ultra-Conserved Poison Exons Enable Rapid and Safe Splicing Factor Gene Expression Switches: A Hypothesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Integrated spatial morpho-transcriptomics predicts functional traits in pancreatic cancer.Science advances · 2025Article
- Dual Role of Transformer 2 Beta as Both a Developmental Necessity and a Disease Modulator.International journal of molecular sciences · 2025Review
- SRC Kinase Isoforms Regulate mRNA Splicing during Neural Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A homozygous human WNT11 variant is associated with laterality, heart and renal defects.Disease models & mechanisms · 2025Article
- Splicing to orchestrate cell fate.Molecular therapy. Nucleic acids · 2025Review
- Bulk and single-cell alternative splicing analyses reveal roles of TRA2B in myogenic differentiation.Cell proliferation · 2024Article
- Moderate maternal nutrient reduction in pregnancy alters fatty acid oxidation and RNA splicing in the nonhuman primate fetal liver.Journal of developmental origins of health and disease · 2023Article
- The Role of Splicing Factors in Adipogenesis and Thermogenesis.Molecules and cells · 2023Review
- Alternative splicing shapes the transcriptome complexity in blackgram [Vigna mungo (L.) Hepper].Functional & integrative genomics · 2023Article
- Maternal Wnt11b regulates cortical rotation during Xenopus axis formation: analysis of maternal-effect wnt11b mutants.Development (Cambridge, England) · 2022Article
- Switched alternative splicing events as attractive features in lung squamous cell carcinoma.Cancer cell international · 2022Article
- Proteomic Analysis of Exosomes during Cardiogenic Differentiation of Human Pluripotent Stem Cells.Cells · 2021Article
- Evolution of Somite Compartmentalization: A View FromFrontiers in cell and developmental biology · 2021Article
- Poison Exon Splicing Regulates a Coordinated Network of SR Protein Expression during Differentiation and Tumorigenesis.Molecular cell · 2020Article
- Arsenite Exposure Displaces Zinc from ZRANB2 Leading to Altered Splicing.Chemical research in toxicology · 2020Article
- Bi-allelic ADARB1 Variants Associated with Microcephaly, Intellectual Disability, and Seizures.American journal of human genetics · 2020Article
- Article
- The Multifaceted Role of HSF1 in Tumorigenesis.Advances in experimental medicine and biology · 2020Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Alternative splicing is pervasive in vertebrates, yet little is known about most isoforms or their regulation. transformer-2b (tra2b) encodes a splicing regulator whose endogenous function is poorly understood. Tra2b knockdown in Xenopus results in embryos with multiple defects, including defective somitogenesis. Using RNA sequencing, we identify 142 splice changes (mostly intron retention and exon skipping), 89% of which are not in current annotations. A previously undescribed isoform of wnt11b retains the last intron, resulting in a truncated ligand (Wnt11b-short). We show that this isoform acts as a dominant-negative ligand in cardiac gene induction and pronephric tubule formation. To determine the contribution of Wnt11b-short to the tra2b phenotype, we induce retention of intron 4 in wnt11b, which recapitulates the failure to form somites but not other tra2b morphant defects. This alternative splicing of a Wnt ligand adds intricacy to a complex signaling pathway and highlights intron retention as a regulatory mechanism.
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