ArticleDevelopmental biology2025
Rbm8a deficiency causes hematopoietic defects by modulating Wnt/PCP signaling.
Article in Developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TAR syndrome causal gene RBM8A is critical for embryonic bone development and proper Hedgehog signaling.Research square · 2026Article
- TAR syndrome causal genebioRxiv : the preprint server for biology · 2026Article
- Successful Haplo-Hematopoietic Stem Cell Transplantation for Juvenile Myelomonocytic Leukemia in a Child With Underlying Thrombocytopenia-Absent Radius Syndrome: A Unique Case.Cancer reports (Hoboken, N.J.) · 2026Article
- Dorsal forerunner cells transmit epiboly forces to extend the zebrafish notochord.bioRxiv : the preprint server for biology · 2025Article
- RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024Article
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Abstract
Thrombocytopenia-Absent Radius (TAR) syndrome is a rare congenital condition with reduced platelets, forelimb anomalies, and variable heart and kidney defects. TAR syndrome is caused by mutations in RBM8A/Y14, a component of the exon junction complex. How perturbing a general mRNA-processing factor causes the selective TAR Syndrome phenotypes remains unknown. Here, we connect zebrafish rbm8a perturbation to early hematopoietic defects via attenuated non-canonical Wnt/Planar Cell Polarity (PCP) signaling. In hypomorphic rbm8a zebrafish, we observe a reduction of cd41-positive thrombocytes. rbm8a-mutant zebrafish accumulate mRNAs with retained introns, including non-canonical Wnt/PCP pathway components resulting in convergent extension defects. We found that reduced rbm8a function interacts with perturbations in non-canonical Wnt/PCP pathway genes wnt5b, wnt11f2, fzd7a, and vangl2, impairing the architecture of the lateral plate mesoderm (LPM) that forms hematopoietic, cardiovascular, kidney, and forelimb skeleton progenitors. Both mutants for rbm8a and for the PCP gene vangl2 feature impaired expression of early hematopoietic/endothelial genes runx1 and gfi1aa. Together, our data propose aberrant LPM patterning and hematopoietic defects as consequence of attenuated non-canonical Wnt/PCP signaling upon reduced rbm8a function.
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