ArticleFrontiers in cell and developmental biology2020
Alpha-Catulin, a New Player in a Rho Dependent Apical Constriction That Contributes to the Mouse Neural Tube Closure.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Emerging Roles of the α-Catenin Family Member α-Catulin in Development, Homeostasis and Cancer Progression.International journal of molecular sciences · 2022Review
- Catulin reporter marks a heterogeneous population of invasive breast cancer cells with some demonstrating plasticity and participating in vascular mimicry.Scientific reports · 2022Article
- Catulin Based Reporter System to Track and Characterize the Population of Invasive Cancer Cells in the Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2021Article
- Intrinsic Mechanical Cues and Their Impact on Stem Cells and Embryogenesis.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coordination of actomyosin contraction and cell-cell junctions generates forces that can lead to tissue morphogenetic processes like the formation of neural tube (NT), however, its molecular mechanisms responsible for regulating and coupling this contractile network to cadherin adhesion remain to be fully elucidated. Here, using a gene trapping technology, we unveil the new player in this process, α-catulin, which shares sequence homology with vinculin and α-catenin. Ablation of α-catulin in mouse causes defective NT closure due to impairment of apical constriction, concomitant with apical actin and P-Mlc2 accumulation. Using a 3D culture model system, we showed that α-catulin localizes to the apical membrane and its removal alters the distribution of active RhoA and polarization. Actin cytoskeleton and P-Mlc2, downstream targets of RhoA, are not properly organized, with limited accumulation at the junctions, indicating a loss of junction stabilization. Our data suggest that α-catulin plays an important role during NT closure by acting as a scaffold for RhoA distribution, resulting in proper spatial activation of myosin to influence actin-myosin dynamics and tension at cell-cell adhesion.
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Registered trials
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