p120 Catenin Is Required for the Stress Response in Drosophila

Stefanatos, Rhoda; Bauer, Christin; Vidal, Marcos

doi:10.1371/journal.pone.0083942

Cited by 7 publications

(8 citation statements)

References 40 publications

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“…Neither temperature nor blocking endocytosis altered mechanical stress at these developmental times ( Figure S4F). To examine the influence of mechanical stress on the endocytosis-dependent pool of Ecad, we performed FRAP analysis 10 min after shifting wildtype or shi ts mutant wings to 34 C at different times of morphogenesis (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40). The difference between F m in wild-type and shi ts at 34 C, a measure of the contribution of endocytosis to F m , significantly decreased with the decrease in mechanical stress between 22 and 40 hAPF ( Figures 4E, 4F, and S4E).…”

Section: Mechanical Stress Modulates Endocytosis-mediated Ecadherin Tmentioning

confidence: 99%

“…To investigate whether the stress dependence of E-cadherin turnover depended on p120, we performed FRAP analysis of E-cad in a p120-null mutant (p120 308 ) [33,37]. In wild-type wings, the minute-scale recovery fraction decreases as mechanical stress decreases during morphogenesis ( Figures 6A and S5).…”

Section: Mechanosensitivity Of E-cadherin Turnover Is Lost In P120 Mumentioning

confidence: 99%

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Epithelial Viscoelasticity Is Regulated by Mechanosensitive E-cadherin Turnover

et al. 2019

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Graphical AbstractHighlights d Mechanical stress releases p120-catenin from apical junctions d Loss of p120-catenin increases endocytic E-cadherin turnover d Loss of p120 speeds stress-dependent remodeling of the junctional network d Mechanical stress dependence of E-cadherin turnover sets tissue viscoelasticity SUMMARY Studying how epithelia respond to mechanical stresses is key to understanding tissue shape changes during morphogenesis. Here, we study the viscoelastic properties of the Drosophila wing epithelium during pupal morphogenesis by quantifying mechanical stress and cell shape as a function of time. We find a delay of 8 h between maximal tissue stress and maximal cell elongation, indicating a viscoelastic deformation of the tissue. We show that this viscoelastic behavior emerges from the mechanosensitivity of endocytic E-cadherin turnover. The increase in E-cadherin turnover in response to stress is mediated by mechanosensitive relocalization of the E-cadherin binding protein p120-catenin (p120) from cell junctions to cytoplasm. Mechanosensitivity of E-cadherin turnover is lost in p120 mutant wings, where E-cadherin turnover is constitutively high. In this mutant, the relationship between mechanical stress and stress-dependent cell dynamics is altered. Cells in p120 mutant deform and undergo cell rearrangements oriented along the stress axis more rapidly in response to mechanical stress. These changes imply a lower viscosity of wing epithelium. Taken together, our findings reveal that p120-dependent mechanosensitive E-cadherin turnover regulates viscoelastic behavior of epithelial tissues.

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Section: Mechanical Stress Modulates Endocytosis-mediated Ecadherin Tmentioning

confidence: 99%

Section: Mechanosensitivity Of E-cadherin Turnover Is Lost In P120 Mumentioning

confidence: 99%

Epithelial Viscoelasticity Is Regulated by Mechanosensitive E-cadherin Turnover

et al. 2019

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“…To investigate whether mechanosensitive binding of p120 to E-Cad regulates E-Cad turnover during pupal morphogenesis, we performed FRAP analysis of E-Cad in a p120 null mutant (p120 308 ) (Myster et al, 2003;Stefanatos et al, 2013). In wild-type wings the minute-scale recovery fraction decreases as mechanical stress decreases during morphogenesis ( Figures 6A, 6B and Figure S12).…”

Section: P120 Regulates Mechanosensitive E-cadherin Turnover and Thermentioning

confidence: 99%

Mechanosensitive binding of p120-Catenin at cell junctions regulates E-Cadherin turnover and epithelial viscoelasticity

Iyer

Piscitello-Gómez

Jülicher

et al. 2018

Preprint

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Studying how epithelia respond to mechanical stresses is key to understanding tissue shape changes during morphogenesis. Here, we study the viscoelastic deformation of the Drosophila pupal wing epithelium in response to mechanical stress that evolves during morphogenesis. We show that wing epithelial tissue viscoelasticity depends on endocytic turnover of E-Cadherin. The fraction of E-Cadherin undergoing turnover depends on mechanical stress in the epithelium.We identified mechanosensitive binding of the endocytic regulator p120-Catenin (p120) as a mechanism to regulate E-Cadherin turnover. Under high stress, p120 is released into the cytoplasm, destabilizing E-Cadherin complexes and increasing its turnover. In p120 mutants, E-Cadherin turnover is insensitive to mechanical stress. Furthermore, we show that p120 is crucial for the viscoelastic deformation of the wing epithelium. Taken together, our findings reveal that mechanosensitive binding of p120-Catenin tunes epithelial tissue viscoelasticity during morphogenesis.

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“…In C. elegans and Drosophila, p120 is considered dispensable, as genetically null adults are clearly viable (Fox et al, 2005;Myster et al, 2003;Pacquelet et al, 2003;Pettitt et al, 2003), albeit sensitive to stress (Stefanatos et al, 2013). In contrast, p120 gene ablation in vertebrates is embryonic lethal.…”

Section: Introductionmentioning

confidence: 99%

p120-catenin controls contractility along the vertical axis of epithelial lateral membranes

Dohn

Markham

et al. 2016

Journal of Cell Science

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In vertebrate epithelia, p120-catenin (hereafter referred to as p120; also known as CTNND1) mediates E-cadherin stability and suppression of RhoA. Genetic ablation of p120 in various epithelial tissues typically causes striking alterations in tissue function and morphology. Although these effects could very well involve p120's activity towards Rho, ascertaining the impact of this relationship has been complicated by the fact that p120 is also required for cell-cell adhesion. Here, we have molecularly uncoupled p120's cadherin-stabilizing and RhoA-suppressing activites. Unexpectedly, removing p120's Rho-suppressing activity dramatically disrupted the integrity of the apical surface, irrespective of E-cadherin stability. The physical defect was tracked to excessive actomyosin contractility along the vertical axis of lateral membranes. Thus, we suggest that p120's distinct activities towards E-cadherin and Rho are molecularly and functionally coupled and this, in turn, enables the maintenance of cell shape in the larger context of an epithelial monolayer. Importantly, local suppression of contractility by cadherin-bound p120 appears to go beyond regulating cell shape, as loss of this activity also leads to major defects in epithelial lumenogenesis.

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p120 Catenin Is Required for the Stress Response in Drosophila

Cited by 7 publications

References 40 publications

Epithelial Viscoelasticity Is Regulated by Mechanosensitive E-cadherin Turnover

Epithelial Viscoelasticity Is Regulated by Mechanosensitive E-cadherin Turnover

Mechanosensitive binding of p120-Catenin at cell junctions regulates E-Cadherin turnover and epithelial viscoelasticity

p120-catenin controls contractility along the vertical axis of epithelial lateral membranes

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