ArticleDevelopment (Cambridge, England)2013
Activin receptor inhibition by Smad2 regulates Drosophila wing disc patterning through BMP-response elements.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Review
- Drosophila activins adapt gut size to food intake and promote regenerative growth.Nature communications · 2024Article
- Article
- A juxtamembrane basolateral targeting motif regulates signaling through a TGF-β pathway receptor in Drosophila.PLoS biology · 2022Article
- pVHL-mediated SMAD3 degradation suppresses TGF-β signaling.The Journal of cell biology · 2022Article
- Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin.Developmental cell · 2021Article
- Muscle-derived Myoglianin regulateseLife · 2020Article
- Article
- Muscle-derived Dpp regulates feeding initiation via endocrine modulation of brain dopamine biosynthesis.Genes & development · 2020Article
- The BMP2/4 ortholog Dpp can function as an inter-organ signal that regulates developmental timing.Life science alliance · 2018Article
- Regulation of neuroblast proliferation by surface glia in the Drosophila larval brain.Scientific reports · 2018Article
- Targeting TGF-β Signaling for Therapeutic Gain.Cold Spring Harbor perspectives in biology · 2017Review
- TGF-β Family Signaling inCold Spring Harbor perspectives in biology · 2017Review
- Regulation of Drosophila hematopoietic sites by Activin-β from active sensory neurons.Nature communications · 2017Article
- TGF-β signaling in insects regulates metamorphosis via juvenile hormone biosynthesis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- CTCF-dependent co-localization of canonical Smad signaling factors at architectural protein binding sites in D. melanogaster.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Strategies for exploring TGF-β signaling in Drosophila.Methods (San Diego, Calif.) · 2014Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Imaginal disc development in Drosophila requires coordinated cellular proliferation and tissue patterning. In our studies of TGFβ superfamily signaling components, we found that a protein null mutation of Smad2, the only Activin subfamily R-Smad in the fruit fly, produces overgrown wing discs that resemble gain of function for BMP subfamily signaling. The wing discs are expanded specifically along the anterior-posterior axis, with increased proliferation in lateral regions. The morphological defect is not observed in mutants for the TGFβ receptor baboon, and epistasis tests showed that baboon is epistatic to Smad2 for disc overgrowth. Rescue experiments indicate that Baboon binding, but not canonical transcription factor activity, of Smad2 is required for normal disc growth. Smad2 mutant discs generate a P-Mad stripe that is narrower and sharper than the normal gradient, and activation targets are correspondingly expressed in narrowed domains. Repression targets of P-Mad are profoundly mis-regulated, with brinker and pentagone reporter expression eliminated in Smad2 mutants. Loss of expression requires a silencer element previously shown to be controlled by BMP signaling. Epistasis experiments show that Baboon, Mad and Schnurri are required to mediate the ectopic silencer output in the absence of Smad2. Taken together, our results show that loss of Smad2 permits promiscuous Baboon activity, which represses genes subject to control by Mad-dependent silencer elements. The absence of Brinker and Pentagone in Smad2 mutants explains the compound wing disc phenotype. Our results highlight the physiological relevance of substrate inhibition of a kinase, and reveal a novel interplay between the Activin and BMP pathways.
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Registered trials
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.