ArticleScientific reports2014
Mad linker phosphorylations control the intensity and range of the BMP-activity gradient in developing Drosophila tissues.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Distinct effects of CDK8 module subunits on cellular growth and proliferation in Drosophila.Development (Cambridge, England) · 2024Article
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- Decapentaplegic Acutely Defines the Connectivity of Central Pacemaker Neurons inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- All-Atomic Molecular Dynamic Studies of Human andInternational journal of molecular sciences · 2020Article
- The Mediator CDK8-Cyclin C complex modulates Dpp signaling in Drosophila by stimulating Mad-dependent transcription.PLoS genetics · 2020Article
- Tao Negatively Regulates BMP Signaling During Neuromuscular Junction Development in Drosophila.Developmental neurobiology · 2019Article
- Understanding Obesity as a Risk Factor for Uterine Tumors Using Drosophila.Advances in experimental medicine and biology · 2019Review
- CDK8 mediates the dietary effects on developmental transition in Drosophila.Developmental biology · 2018Article
- Hippo, TGF-β, and Src-MAPK pathways regulate transcription of the upd3 cytokine in Drosophila enterocytes upon bacterial infection.PLoS genetics · 2017Article
- Drosophila Dullard functions as a Mad phosphatase to terminate BMP signaling.Scientific reports · 2016Article
- CDK8-Cyclin C Mediates Nutritional Regulation of Developmental Transitions through the Ecdysone Receptor in Drosophila.PLoS biology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The BMP ligand Dpp, operates as a long range morphogen to control many important functions during Drosophila development from tissue patterning to growth. The BMP signal is transduced intracellularly via C-terminal phosphorylation of the BMP transcription factor Mad, which forms an activity gradient in developing embryonic tissues. Here we show that Cyclin dependent kinase 8 and Shaggy phosphorylate three Mad linker serines. We demonstrate that linker phosphorylations control the peak intensity and range of the BMP signal across rapidly developing embryonic tissues. Shaggy knockdown broadened the range of the BMP-activity gradient and increased high threshold target gene expression in the early embryo, while expression of a Mad linker mutant in the wing disc resulted in enhanced levels of C-terminally phosphorylated Mad, a 30% increase in wing tissue, and elevated BMP target genes. In conclusion, our results describe how Mad linker phosphorylations work to control the peak intensity and range of the BMP signal in rapidly developing Drosophila tissues.
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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.