ArticleMammalian genome : official journal of the International Mammalian Genome Society2007
An intronic sequence mutated in flexed-tail mice regulates splicing of Smad5.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
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- The mitochondrial carrier SFXN1 is critical for complex III integrity and cellular metabolism.Cell reports · 2021Article
- Insights into the Roles of the Sideroflexins/SLC56 Family in Iron Homeostasis and Iron-Sulfur Biogenesis.Biomedicines · 2021Review
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- Inflammation induces stress erythropoiesis through heme-dependent activation of SPI-C.Science signaling · 2019Article
- Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5.Frontiers in oncology · 2019Article
- Development and differentiation of the erythroid lineage in mammals.Developmental and comparative immunology · 2016Review
- An activin receptor IIA ligand trap corrects ineffective erythropoiesis in β-thalassemia.Nature medicine · 2014Article
- Macrocytic anemia and mitochondriopathy resulting from a defect in sideroflexin 4.American journal of human genetics · 2013Article
- Review
- Stress erythropoiesis: new signals and new stress progenitor cells.Current opinion in hematology · 2011Review
- Murine erythroid short-term radioprotection requires a BMP4-dependent, self-renewing population of stress erythroid progenitors.The Journal of clinical investigation · 2010Article
- Hypoxia regulates BMP4 expression in the murine spleen during the recovery from acute anemia.PloS one · 2010Article
- Alzheimer's disease: diagnostics, prognostics and the road to prevention.The EPMA journal · 2010Article
- Extramedullary erythropoiesis in the adult liver requires BMP-4/Smad5-dependent signaling.Experimental hematology · 2009Article
- BMP4/Smad5 dependent stress erythropoiesis is required for the expansion of erythroid progenitors during fetal development.Developmental biology · 2008Article
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Authors and funding
7 authors.
Funding
Abstract
Recent work has identified a growing body of evidence that subtle changes in noncoding sequences can result in significant pathology. These mutations, which would have been called silent polymorphisms in the past, affect gene transcription and mRNA splicing and lead to drastic changes in gene expression. Previous work from our lab has characterized the murine flexed-tail (f) mutation, which encodes Smad5, a transcription factor that functions downstream of the receptors for bone morphogenetic proteins (BMPs). f/f mice are unable to rapidly respond to acute anemia. Our analysis of these mice led to the development of a new model for stress erythropoiesis, where BMP4 expression in the spleen leads to the Smad5-dependent expansion of a specialized population of stress erythroid progenitors during the recovery from acute anemia. f/f mutant mice exhibit a defect in Smad5 mRNA splicing in the spleen such that the majority of Smad5 transcripts are two misspliced mRNAs. One of these mRNAs encodes a truncated form of Smad5 that inhibits BMP4 signaling when overexpressed. Here we show that a mutation in a poly(T) element in intron 4 causes the splicing defect in f/f mutant mice. This subtle mutation (loss of 1 or 2 Ts in a 16-T element) results in defects in splicing throughout the Smad5 gene. Furthermore, we show that this mutation results in tissue-specific splicing defects, which may explain why f/f mice are viable when Smad5-/- mice are embryonic lethal.
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