ArticlePLoS genetics2014
The COP9 signalosome converts temporal hormone signaling to spatial restriction on neural competence.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- COP9 signalosome regulates EGFR and Notch signaling during myeloid-type progenitor cell fate decision in Drosophila.EMBO reports · 2026Article
- Systematic analysis of the Frazzled receptor interactome establishes previously unreported regulators of axon guidance.Development (Cambridge, England) · 2023Article
- Nuclear receptors linking physiology and germline stem cells in Drosophila.Vitamins and hormones · 2021Review
- Identification of COP9 Signalosome Subunit Genes inFrontiers in physiology · 2019Article
- Temporospatial induction of homeodomain geneeLife · 2018Article
- Dancing in the dark: darkness as a signal in plants.Plant, cell & environment · 2017Review
- The Evolution of COP9 Signalosome in Unicellular and Multicellular Organisms.Genome biology and evolution · 2016Article
- Modeling congenital disease and inborn errors of development in Drosophila melanogaster.Disease models & mechanisms · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During development, neural competence is conferred and maintained by integrating spatial and temporal regulations. The Drosophila sensory bristles that detect mechanical and chemical stimulations are arranged in stereotypical positions. The anterior wing margin (AWM) is arrayed with neuron-innervated sensory bristles, while posterior wing margin (PWM) bristles are non-innervated. We found that the COP9 signalosome (CSN) suppresses the neural competence of non-innervated bristles at the PWM. In CSN mutants, PWM bristles are transformed into neuron-innervated, which is attributed to sustained expression of the neural-determining factor Senseless (Sens). The CSN suppresses Sens through repression of the ecdysone signaling target gene broad (br) that encodes the BR-Z1 transcription factor to activate sens expression. Strikingly, CSN suppression of BR-Z1 is initiated at the prepupa-to-pupa transition, leading to Sens downregulation, and termination of the neural competence of PWM bristles. The role of ecdysone signaling to repress br after the prepupa-to-pupa transition is distinct from its conventional role in activation, and requires CSN deneddylating activity and multiple cullins, the major substrates of deneddylation. Several CSN subunits physically associate with ecdysone receptors to represses br at the transcriptional level. We propose a model in which nuclear hormone receptors cooperate with the deneddylation machinery to temporally shutdown downstream target gene expression, conferring a spatial restriction on neural competence at the PWM.
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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.