Cell–cell adhesion is a fundamental feature of multicellular organisms. To ensure multicellular integrity, adhesion needs to be tightly controlled and maintained. In plants, cell–cell adhesion remains poorly understood. Here, we argue that to be able to understand how cell–cell adhesion works in plants, we need to understand and quantitatively measure the mechanics behind it. We first introduce cell–cell adhesion in the context of multicellularity, briefly explain the notions of adhesion strength, work and energy and present the current knowledge concerning the mechanisms of cell–cell adhesion in plants. Because still relatively little is known in plants, we then turn to animals, but also algae, bacteria, yeast and fungi, and examine how adhesion works and how it can be quantitatively measured in these systems. From this, we explore how the mechanics of cell adhesion could be quantitatively characterised in plants, opening future perspectives for understanding plant multicellularity.

Electro-osmosis phenomena are studied in a two-dimensional (2D) model disordered porous medium. The flow passages are represented by a network of spatially distributed rectangular channels with random orientations. The channels may represent microfractures in fractured porous media or in a network of interconnected microfractures, pores in a porous medium, or fibers in a fibrous porous material. The linearized equations of electrokinetics are solved numerically in a single channel, and in the 2D network of the channels. The macroscopic electrical conductivity σ and electro-osmotic coupling coefficient β are computed as functions of the electrical surface potential ζ and such geometrical parameters of the network as the channels' number density and widths, as well as the porosity of the medium. Despite the complexity of the phenomena and the model of porous media that is used, both σ and β appear to depend on the characteristics of the phenomena and porous media through very simple relations.

The forces that arise from the actin cortex play a crucial role in determining the membrane deformation. These include protrusive forces due to actin polymerization, pulling forces due to transient attachment of actin filaments to the membrane, retrograde flow powered by contraction of actomyosin network, and adhesion to the extracellular matrix. Here we present a theoretical model for membrane deformation resulting from the feedback between the membrane shape and the forces acting on the membrane. We model the membrane as a series of beads connected by springs and determine the final steady-state shape of the membrane arising from the interplay between pushing/pulling forces of the actin network and the resisting membrane tension. We specifically investigate the effect of the gel dynamics on the spatio-temporal deformation of the membrane until a stable lamellipodium is formed. We show that the retrograde flow and the cross-linking velocity play an essential role in the final elongation of the membrane. Interestingly, in the simulations where motor-induced contractility is switched off, reduced retrograde flow results in an increase in the rate and amplitude of membrane protrusion. These simulations are consistent with experimental observations that report an enhancement in protrusion efficiency as myosin II molecular motors are inhibited.

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