Journal
SCIENCE
Volume 307, Issue 5708, Pages 423-426Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1105471
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Funding
- NIGMS NIH HHS [R01-GM59823] Funding Source: Medline
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Planar cell polarity (PCP) signaling generates subcellular asymmetry along an axis orthogonal to the epithelia[ apical-basal axis. Through a poorly understood mechanism, cell clones that have mutations in some PCP signaling components, including some, but not all, alleles of the receptor frizzled, cause polarity disruptions of neighboring wild-type cells, a phenomenon referred to as domineering nonautonomy. Here, a contact-dependent signaling hypothesis, derived from experimental results, is shown by reaction-diffusion, partial differential equation modeling and simulation to fully reproduce PCP phenotypes, including domineering nonautonomy, in the Drosophila wing. The sufficiency of this model and the experimental validation of model predictions reveal how specific protein-protein interactions produce autonomy or domineering nonautonomy.
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