ArticlePLoS genetics2013
Strabismus promotes recruitment and degradation of farnesylated prickle in Drosophila melanogaster planar polarity specification.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- PRICKLE3 protects VANGL proteins from CK1-mediated phosphorylation and RNF43-mediated degradation.Communications biology · 2025Article
- Article
- Evaluating protein prenylation of human and viral CaaX sequences using a humanized yeast system.Disease models & mechanisms · 2024Article
- Planar Cell Polarity Signaling: Coordinated Crosstalk for Cell Orientation.Journal of developmental biology · 2024Review
- A Humanized Yeast System for Evaluating the Protein Prenylation of a Wide Range of Human and Viral CaaX Sequences.bioRxiv : the preprint server for biology · 2023Article
- A Van Gogh/Vangl tyrosine phosphorylation switch regulates its interaction with core Planar Cell Polarity factors Prickle and Dishevelled.PLoS genetics · 2023Article
- Distinct mechanisms of planar polarization by the core and Fat-Dachsous planar polarity pathways in the Drosophila wing.Cell reports · 2022Article
- Article
- How do the Fat-Dachsous and core planar polarity pathways act together and independently to coordinate polarized cell behaviours?Open biology · 2021Review
- Molecular mechanisms mediating asymmetric subcellular localisation of the core planar polarity pathway proteins.Biochemical Society transactions · 2020Review
- DAnkrd49 and Bdbt act via Casein kinase Iε to regulate planar polarity in Drosophila.PLoS genetics · 2020Article
- Article
- Wnt/PCP Signaling Contribution to Carcinoma Collective Cell Migration and Metastasis.Cancer research · 2019Review
- Vangl2 interaction plays a role in the proteasomal degradation of Prickle2.Scientific reports · 2019Article
- Rapid Disruption of Dishevelled Activity Uncovers an Intercellular Role in Maintenance of Prickle in Core Planar Polarity Protein Complexes.Cell reports · 2018Article
- Cellular and molecular mechanisms underlying planar cell polarity pathway contributions to cancer malignancy.Seminars in cell & developmental biology · 2018Review
- Prickle is phosphorylated by Nemo and targeted for degradation to maintain Prickle/Spiny-legs isoform balance during planar cell polarity establishment.PLoS genetics · 2018Article
- From instruction to output: Wnt/PCP signaling in development and cancer.Current opinion in cell biology · 2018Review
- A Dual Function for Prickle in Regulating Frizzled Stability during Feedback-Dependent Amplification of Planar Polarity.Current biology : CB · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The core planar polarity proteins are required to specify the orientation of structures that are polarised in the plane of the epithelium. In the Drosophila melanogaster wing, the core proteins localise asymmetrically at either proximal or distal cell edges. Asymmetric localisation is thought to be biased by long-range cues, causing asymmetric complexes to become aligned with the tissue axes. Core proteins are then thought to participate in feedback interactions that are necessary to amplify asymmetry, and in order for such feedback interactions to operate correctly, the levels of the core proteins at junctions must be tightly regulated. We have investigated regulation of the core protein Prickle (Pk) in the pupal wing. The core protein Strabismus (Stbm) is required to recruit Pk into asymmetric complexes at proximal cell ends, and we report here that it also promotes proteasomal degradation of excess Pk, probably via a Cullin-1 dependent process. We also show for the first time that Pk is farnesylated in vivo, and this is essential for Pk function in the wing. Notably, farnesylation of Pk is necessary for it to be recruited into asymmetric complexes and function in feedback amplification, probably by reinforcing weak direct interactions between Stbm and Pk. Furthermore, farnesylation is also required for Stbm to promote proteasomal degradation of Pk. We propose that Stbm recruits farnesylated Pk into asymmetric complexes, but also promotes degradation of excess Pk that would otherwise perturb feedback amplification.
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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.