Cell motion and mechanobiology.

Abstract

Diverse new and stimulating results at the interfaces between cell and molecular biology and biophysics were presented in this session cochaired by Ewa Paluch (University College London) and Dennis Discher (University of Pennsylvania). A number of physical features of the cell and its microenvironment were shown to impact the functions and fates of diverse cell types. Five talks of standard length ranged across the topics of adhesive sensing of matrix rigidity to migration without adhesions in three dimensions, and these were followed by six “lightning talks” that ranged in focus from the role of the nucleus in three-dimensional (3D) motility to osmotic effects on migration. Quantitative microscopic analyses of tension-sensitive fluorescence resonance energy transfer (FRET) sensors were presented by Alex Dunn and coworkers (Stanford University) in studies aimed at clarifying the nanoscale architecture of tension generation within integrin focal adhesions. Such structures are classically seen when cells adhere to rigid but not soft substrates, and Corinne Albiges-Rizo and colleagues (Institut Albert Bonniot, Grenoble) described their work on how integrin-mediated sensitivity of mesenchymal cells to matrix rigidity is also altered by the differentiation factor BMP2 when it is bound to matrix—as often occurs in vivo. Past and present physical approaches to clarifying how matrix-rigidity sensing drives actin cytoskeleton remodeling and rheology within various tissue cells was elaborated by Benoit Ladoux and coworkers (Ladoux and Nicolas, 2012 ) (Mechanobiology Institute, Singapore, and Universite Paris Diderot). The migratory behavior of primary dendritic cells in confined environments was explained in terms of an Arp2/3 to formin switch that is key to adapting these cells to their function upon maturation in a talk by Ana-Maria Lennon-Dumenil (Institut Curie, Paris). The generation and magnitude of forces driving 3D migration of cancer cells unable to form focal adhesions was then presented by Ewa Paluch (Bergert et al., 2015 ), completing the first half of the session. The first “lightning talk” extended the 3D motility theme to evidence that a cancer cell can pull on its nucleus with such strength that it can damage its own lamina and cause DNA breaks, according to Jerome Irianto and coworkers (University of Pennsylvania; Harada et al., 2014 ). Caren Norden and coworkers (Max Planck Institute of Molecular Cell Biology and Genetics, Dresden) extended the 3D theme to microtubule contributions to migration of a neuron's soma in vivo and somal translocation, while Ryan Petrie and colleagues (National Institutes of Health, Bethesda) described the nucleus as a piston that is pulled forward by myosin II in fibroblasts to increase intracellular pressure at the cell front and drive 3D cell movement (Petrie et al., 2014 ). Cheng-han Yu (University of Hong Kong, and Mechanobiology Institute, Singapore) returned to earlier themes of adhesion in describing mechanisms for how, in the absence of traction force, integrin β3 clusters recruit clathrin-mediated endocytic machinery. The session finished with talks on osmotic sensing in 3D migration. First, William Gault and coworkers (Sloan-Kettering Institute, New York) discussed how epidermal cells in larval zebrafish tail fins take osmotic cues from the environment for rapid detection of epithelial breaches (Gault et al., 2014 ). They were followed by Kostas Konstantopoulos (Johns Hopkins University, Baltimore), who provided evidence from studies of cells in 3D channels for the role of an osmotic engine in migration (Stroka et al., 2014 ).