ArticleMolecular and cellular biology2004
Functional studies of shaggy/glycogen synthase kinase 3 phosphorylation sites in Drosophila melanogaster.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 63 citations in OpenAlex.
- The Evolutionary Flexibility of the Drosophila Circadian Clock: Network Constraints or Adaptive Freedom?Genome biology and evolution · 2026Article
- Diabetic sensory neuropathy and insulin resistance are induced by loss of UCHL1 in Drosophila.Nature communications · 2024Article
- The diverse roles of insulin signaling in insect behavior.Frontiers in insect science · 2024Review
- Feedback in the β-catenin destruction complex imparts bistability and cellular memory.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Shaggy regulates tissue growth through Hippo pathway in Drosophila.Science China. Life sciences · 2022Article
- Modulated Expression of the Protein Kinase GSK3 in Motor and Dopaminergic Neurons Increases Female Lifespan inFrontiers in genetics · 2020Article
- Characterisation of protein isoforms encoded by the Drosophila Glycogen Synthase Kinase 3 gene shaggy.PloS one · 2020Article
- Destruction complex dynamics: Wnt/β-catenin signaling alters Axin-GSK3β interactionsDevelopment (Cambridge, England) · 2019Article
- Triacylglycerol Metabolism inGenetics · 2018Review
- The bHLH Protein Nulp1 is Essential for Femur Development Via Acting as a Cofactor in Wnt Signaling in Drosophila.Current molecular medicine · 2018Article
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- The Indirubin Derivative 6-Bromoindirubin-3'-Oxime Activates Proteostatic Modules, Reprograms Cellular Bioenergetic Pathways, and Exerts Antiaging Effects.Antioxidants & redox signaling · 2017Article
- 6-bromo-indirubin-3'-oxime (6BIO), a Glycogen synthase kinase-3β inhibitor, activates cytoprotective cellular modules and suppresses cellular senescence-mediated biomolecular damage in human fibroblasts.Scientific reports · 2017Article
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- GSK-3 signaling in developing cortical neurons is essential for radial migration and dendritic orientation.eLife · 2014Article
- New X-chromosomal interactors of dFMRP regulate axonal and synaptic morphology of brain neurons inBiotechnology, biotechnological equipment · 2014Article
- Lithium chloride alleviates neurodegeneration partly by inhibiting activity of GSK3β in a SCA3 Drosophila model.Cerebellum (London, England) · 2013Article
- Loss of the starvation-induced gene Rack1 leads to glycogen deficiency and impaired autophagic responses in Drosophila.Autophagy · 2012Article
- The kinase Sgg modulates temporal development of macrochaetes in Drosophila by phosphorylation of Scute and Pannier.Development (Cambridge, England) · 2012Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early studies of glycogen synthase kinase 3 (GSK-3) in mammalian systems focused on its pivotal role in glycogen metabolism and insulin-mediated signaling. It is now recognized that GSK-3 is central to a number of diverse signaling systems. Here, we show that the major form of the kinase Shaggy (Sgg), the GSK-3 fly ortholog, is negatively regulated during insulin-like/phosphatidylinositol 3-kinase (PI3K) signaling in vivo. Since genetic studies of Drosophila melanogaster had previously shown that Wingless (Wg) signaling also acts to antagonize Sgg, we investigate how the kinase might integrate, or else discriminate, signaling inputs by Wg and insulin. Using Drosophila cell line assays, we found, in contrast to previous reports, that Wg induces accumulation of its transducer Armadillo (Arm)/beta-catenin without significant alteration of global Sgg-specific activity. In agreement with a previous study using human GSK-3beta, Wg did not cause phosphorylation changes of the Ser9 or Tyr214 regulatory phosphorylated sites of Sgg. Conversely, as shown in mammalian systems, insulin-induced inhibition of Sgg-specific activity by phosphorylation at the N-terminal pseudosubstrate site (Ser9) did not induce Arm/beta-catenin accumulation, showing selectivity in response to the different signaling pathways. Interestingly, a minigene bearing a Ser9-to-Ala change rescued mutant sgg without causing abnormal development, suggesting that the regulation of Sgg via the inhibitory pseudosubstrate domain is dispensable for many aspects of its function. Our studies of Drosophila show that Wg and insulin or PI3K pathways do not converge on Sgg but that they exhibit cross-regulatory interactions.
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