ArticleGenetics2007
The nonmuscle myosin phosphatase PP1beta (flapwing) negatively regulates Jun N-terminal kinase in wing imaginal discs of Drosophila.
Article in Genetics, 2007. 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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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Hippo signaling regulates cuticle pigmentation and dopamine metabolism in Drosophila.PLoS genetics · 2026Article
- From network analysis to experimental validation: identification of regulators of non-muscle myosin II contractility using the folded-gastrulation signaling pathway.BMC molecular and cell biology · 2023Article
- Actomyosin contractility modulates Wnt signaling through adherens junction stability.Molecular biology of the cell · 2019Article
- Ligand-Bound GeneSwitch Causes Developmental Aberrations in Drosophila that Are Alleviated by the Alternative Oxidase.G3 (Bethesda, Md.) · 2016Article
- Myosin light-chain phosphatase regulates basal actomyosin oscillations during morphogenesis.Nature communications · 2016Article
- Greatwall-phosphorylated Endosulfine is both an inhibitor and a substrate of PP2A-B55 heterotrimers.eLife · 2014Article
- In Drosophila, RhoGEF2 cooperates with activated Ras in tumorigenesis through a pathway involving Rho1-Rok-Myosin-II and JNK signalling.Disease models & mechanisms · 2013Article
- Sds22/PP1 links epithelial integrity and tumor suppression via regulation of myosin II and JNK signaling.Oncogene · 2011Article
- Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II.Developmental biology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Drosophila flapwing (flw) codes for serine/threonine protein phosphatase type 1beta (PP1beta). Regulation of nonmuscle myosin activity is the single essential flw function that is nonredundant with the three closely related PP1alpha genes. Flw is thought to dephosphorylate the nonmuscle myosin regulatory light chain, Spaghetti Squash (Sqh); this inactivates the nonmuscle myosin heavy chain, Zipper (Zip). Thus, strong flw mutants lead to hyperphosphorylation of Sqh and hyperactivation of nonmuscle myosin activity. Here, we show genetically that a Jun N-terminal kinase (JNK) mutant suppresses the semilethality of a strong flw allele. Alleles of the JNK phosphatase puckered (puc) genetically enhance the weak allele flw1, leading to severe wing defects. Introducing a mutant of the nonmuscle myosin-binding subunit (Mbs) further enhances this genetic interaction to lethality. We show that puc expression is upregulated in wing imaginal discs mutant for flw1 and pucA251 and that this upregulation is modified by JNK and Zip. The level of phosphorylated (active) JNK is elevated in flw1 enhanced by puc. Together, we show that disruption of nonmuscle myosin activates JNK and puc expression in wing imaginal discs.
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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.