ArticleMolecular biology and evolution2014
New gene evolution in the bonus-TIF1-γ/TRIM33 family impacted the architecture of the vertebrate dorsal-ventral patterning network.
Article in Molecular biology and evolution, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 13 citations in OpenAlex.
- Multi-omics integration highlights the role of ubiquitination in endometriosis fibrosis.Journal of translational medicine · 2024Article
- Review
- Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023Review
- Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye.Developmental cell · 2023Article
- A Case Report of Anti-TIF1-Case reports in rheumatology · 2023Article
- Transgenic Analyses in Drosophila Reveal That mCORL1 Is Functionally Distinct from mCORL2 and dCORL.G3 (Bethesda, Md.) · 2019Article
- USP4 inhibits SMAD4 monoubiquitination and promotes activin and BMP signaling.The EMBO journal · 2017Article
- lolal Is an Evolutionarily New Epigenetic Regulator of dpp Transcription during Dorsal-Ventral Axis Formation.Molecular biology and evolution · 2016Article
- A Comprehensive Transcriptomic and Proteomic Analysis of Hydra Head Regeneration.Molecular biology and evolution · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Uncovering how a new gene acquires its function and understanding how the function of a new gene influences existing genetic networks are important topics in evolutionary biology. Here, we demonstrate nonconservation for the embryonic functions of Drosophila Bonus and its newest vertebrate relative TIF1-γ/TRIM33. We showed previously that TIF1-γ/TRIM33 functions as an ubiquitin ligase for the Smad4 signal transducer and antagonizes the Bone Morphogenetic Protein (BMP) signaling network underlying vertebrate dorsal-ventral axis formation. Here, we show that Bonus functions as an agonist of the Decapentaplegic (Dpp) signaling network underlying dorsal-ventral axis formation in flies. The absence of conservation for the roles of Bonus and TIF1-γ/TRIM33 reveals a shift in the dorsal-ventral patterning networks of flies and mice, systems that were previously considered wholly conserved. The shift occurred when the new gene TIF1-γ/TRIM33 replaced the function of the ubiquitin ligase Nedd4L in the lineage leading to vertebrates. Evidence of this replacement is our demonstration that Nedd4 performs the function of TIF1-γ/TRIM33 in flies during dorsal-ventral axis formation. The replacement allowed vertebrate Nedd4L to acquire novel functions as a ubiquitin ligase of vertebrate-specific Smad proteins. Overall our data reveal that the architecture of the Dpp/BMP dorsal-ventral patterning network continued to evolve in the vertebrate lineage, after separation from flies, via the incorporation of new genes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.