ArticleOpen biology2019
Integrins are required for synchronous ommatidial rotation in the Drosophila eye linking planar cell polarity signalling to the extracellular matrix.
Article in Open biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Interommatidial cells build a tensile collagen network during Drosophila retinal morphogenesis.Current biology : CB · 2023Article
- Function and prognostic value of basement membrane -related genes in lung adenocarcinoma.Frontiers in pharmacology · 2023Article
- Notch-dependent Abl signaling regulates cell motility during ommatidial rotation in Drosophila.Cell reports · 2022Article
- Wnt-frizzled planar cell polarity signaling in the regulation of cell motility.Current topics in developmental biology · 2022Review
- Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation.Nature communications · 2021Article
- A Pan-Cancer Analysis of the Oncogenic Role of Integrin Beta4 (ITGB4) in Human Tumors.International journal of general medicine · 2021Article
- Inhibition of Rho-associated protein kinase improves the survival of human induced pluripotent stem cell-derived cardiomyocytes after dissociation.Experimental and therapeutic medicine · 2020Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Integrins mediate the anchorage between cells and their environment, the extracellular matrix (ECM), and form transmembrane links between the ECM and the cytoskeleton, a conserved feature throughout development and morphogenesis of epithelial organs. Here, we demonstrate that integrins and components of the ECM are required during the planar cell polarity (PCP) signalling-regulated cell movement of ommatidial rotation in the Drosophila eye. The loss-of-function mutations of integrins or ECM components cause defects in rotation, with mutant clusters rotating asynchronously compared to wild-type clusters. Initially, mutant clusters tend to rotate faster, and at later stages they fail to be synchronous with their neighbours, leading to aberrant rotation angles and resulting in a disorganized ommatidial arrangement in adult eyes. We further demonstrate that integrin localization changes dynamically during the rotation process. Our data suggest that core Frizzled/PCP factors, acting through RhoA and Rho kinase, regulate the function/activity of integrins and that integrins thus contribute to the complex interaction network of PCP signalling, cell adhesion and cytoskeletal elements required for a precise and synchronous 90° rotation movement.
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Registered trials
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