Access IBEC scientific production portal (IBEC CRIS), for more detailed information and advanced search features.
Find here the list of all IBEC's publications by year.
by Keyword: Contact inhibition
Zimkowska, Karolina, Riu-Villanueva, Marc, del Rio, Jose A, (2026). Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions Cells 15, 178 
Neuromechanobiology has emerged as a multidisciplinary field at the interface of neuroscience and mechanobiology, aiming to elucidate how mechanical forces influence the development, organization, and function of the nervous system. This review offers a comprehensive overview of the historical evolution of the discipline, its molecular and biophysical foundations, and the experimental strategies employed to investigate it. Recent advances have revealed the pivotal roles of substrate stiffness, mechanical signaling, and force transduction in neural stem proliferation, axon guidance, synapse formation, and neural circuit maturation. All these effects originate at the molecular level and extend to the mesoscopic scale. Disrupted mechanotransduction has been increasingly implicated in neurodevelopmental disorders and neurodegenerative diseases, underscoring its clinical relevance. Key unresolved questions and future directions are also highlighted, with emphasis on the need for integrative approaches to decipher the complex interplay between mechanical forces and neural function.
JTD Keywords: Axon guidance, Brain development, Central-nervous-system, Contact inhibition, Force transmission, Hippo pathway, Human brain-development, Mechanical forces, Mechanical-properties, Mechanotransduction, Neural migration and regional specification, Neuromechanobiology, Patterned neural-tube, Pluripotent stem-cells, Signaling pathway, Synaptic activity, Tau mislocalization
Noordstra, I, Hermoso, MD, Schimmel, L, Bonfim-Melo, A, Currin-Ross, D, Duong, CN, Kalappurakkal, JM, Morris, RG, Vestweber, D, Mayor, S, Gordon, E, Roca-Cusachs, P, Yap, AS, (2023). An E-cadherin-actin clutch translates the mechanical force of cortical flow for cell-cell contact to inhibit epithelial cell locomotion DEVELOPMENTAL CELL 58, 1748-1763
Adherens junctions (AJs) allow cell contact to inhibit epithelial migration yet also permit epithelia to move as coherent sheets. How, then, do cells identify which contacts will inhibit locomotion? Here, we show that in human epithelial cells this arises from the orientation of cortical flows at AJs. When the leader cells from different migrating sheets make head-on contact with one another, they assemble AJs that couple together oppositely directed cortical flows. This applies a tensile signal to the actin-binding domain (ABD) of a-cate-nin, which provides a clutch to promote lateral adhesion growth and inhibit the lamellipodial activity neces-sary for migration. In contrast, AJs found between leader cells in the same migrating sheet have cortical flows aligned in the same direction, and no such mechanical inhibition takes place. Therefore, a-catenin mechano-sensitivity in the clutch between E-cadherin and cortical F-actin allows cells to interpret the direction of motion via cortical flows and signal for contact to inhibit locomotion.
JTD Keywords: Clutch, Contact inhibition of locomotion, Cortical flow, E-cadherin adhesion, Mechanical tension, Α-catenin
Hino, N, Matsuda, K, Jikko, Y, Maryu, G, Sakai, K, Imamura, R, Tsukiji, S, Aoki, K, Terai, K, Hirashima, T, Trepat, X, Matsuda, M, (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration DEVELOPMENTAL CELL 57, 2290-2304
Upon the initiation of collective cell migration, the cells at the free edge are specified as leader cells; however, the mechanism underlying the leader cell specification remains elusive. Here, we show that lamellipodial extension after the release from mechanical confinement causes sustained extracellular signal-regulated kinase (ERK) activation and underlies the leader cell specification. Live-imaging of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use of Förster resonance energy transfer (FRET)-based biosensors showed that leader cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension at the free edge increases the cellular sensitivity to HGF. The HGF-dependent ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive feedback loop between cell extension and ERK activation and specifying the cells at the free edge as the leader cells. Our findings show that the integration of physical and biochemical cues underlies the leader cell specification during collective cell migration.Copyright © 2022 Elsevier Inc. All rights reserved.
JTD Keywords: activation, c-met, contact inhibition, focal adhesions, heparan-sulfate, mechanical forces, morphogenesis, rho, stress fibers, Collective cell migration, Erk, Feedback regulation, Fret, Growth-factor receptor, Hgf, Lamellipodia, Leader cell specification, Signal transduction, Traction force, Wound healing
