arXiv subjects

Boris Martinac

Publications and source records attributed to Boris Martinac.

4 recordsLinked to original sources

arXiv2026

Active wetting/de-wetting of focal adhesions on viscoelastic substrates

Cell adhesion to viscoelastic substrates is mediated by focal adhesions (FAs), which dynamically couple actomyosin contractility to the extracellular matrix. Although substrate stress relaxation is known to regulate adhesion stability and cell migration, a predictive physical framework linking viscoelasticity to force transmission and adhesion dynamics remains lacking. Here we review briefly what is known about the active wetting and de-wetting of FAs on viscoelastic substrates and synthesize existing experimental and theoretical work into a two-timescale physical framework to describe the phenomena reported. At short timescales, oscillatory actomyosin-driven displacements are transmitted through molecular clutches, leading to frequency-dependent energy transfer to the substrate. We show that this transfer is maximized at an optimal frequency set by a balance between elastic energy storage and viscous dissipation, establishing a resonance-like mechanism that selects both the effective FA stiffness and traction force amplitude. At longer timescales, this mechanically optimal state couples to adhesion remodelling through an effective surface tension, enabling FA growth and disassembly to be interpreted as active wetting and de-wetting processes. The model predicts that adhesion stability and steady-state size are controlled by substrate stiffness and viscoelastic timescales, as well as mechanosensitive feedback mediated by Piezo1-dependent calcium signalling.

cond-mat.soft↗

arXiv2026

Irregular curvature at focal adhesions modulates Piezo1 activity and low frequency ultrasound induced apoptosis in cancer cells

Low-frequency, low intensity ultrasound (LIUS) has emerged as a promising physical modality capable of inducing selective apoptosis of cancer cells, while sparing healthy epithelial cells and fibroblasts. Hitherto, the mechanism underlying this selectivity has been unclear, but we now propose and develop a theoretical framework linking the distinct mechanical behaviours of cancer versus healthy cells to their differential responses to LIUS. We point out that cancer cells exhibit inhomogeneous ventral stress-fiber networks, which can produce irregular focal adhesion geometry and inward membrane curvature near focal adhesions under low-intensity ultrasound (LIUS). These curvature irregularities can favor loose packing of Piezo1 channels, thereby preserving their activity. In contrast, healthy epithelial cells and fibroblasts display more homogeneous cytoskeletal organization, which can result in more regular curvature profiles adjacent to focal adhesions. This leads to curvature-driven cholesterol redistribution, resulting in altered spatial organization of Piezo1 clusters and reduced coordinated channel activity and allowing cells to remain in their active, proliferative state when exposed to LIUS. Based on theoretical modeling and previous experimental findings, we propose that differences in cytoskeletal organization and membrane curvature can contribute to distinct Piezo1 activation patterns between healthy and cancerous cells. Our analysis identifies curvature-mediated Piezo1 redistribution as a potential physical basis for LIUS selectivity and provides a mechanistic foundation for designing ultrasound-based therapies to exploit the intrinsic cytoskeletal vulnerabilities of cancer cells.

q-bio.BM↗

arXiv2026

Marangoni-Driven Redistribution and Activity of Piezo1 Molecules in Epithelial and Cancer Cells

The activity and distribution of Piezo1 molecules, along with the maturity and strength of focal adhesions (FAs), serve as critical factors influencing cell mechanosensing. Notably, migrating epithelial cells and mesenchymal-like cancer cells exhibit significantly different behaviors regarding these elements. In cancer cells, Piezo1 molecules are distributed uniformly, while in epithelial cells, their distribution is heterogeneous. In epithelial cells, Piezo1 molecules tend to group around FAs, a phenomenon that is enhanced by actomyosin contractility. However, a reduction in contractility results in a more uniform distribution of Piezo1 molecules. The expression and activity levels of Piezo1 molecules are markedly higher in cancer cells compared to epithelial cells. The activity of Piezo1 molecules correlates with the intracellular calcium concentration. Despite the extensive experimental studies on the properties of migrating epithelial and mesenchymal-like cancer cells, the physical explanations remain lacking. The primary objective of this theoretical study is to explore: (i) the inhomogeneous distribution of Piezo1 molecules in epithelial cells in relation to the Marangoni effect, (ii) the heightened activity of Piezo1 molecules in cancer cells by specifying the driving force, and (iii) the influence of membrane-mediated interactions among Piezo1 molecules grouped near FAs in epithelial cells on their activity.

q-bio.CB↗

arXiv2014

Single Molecule FRET Reveals Pore Size and Opening Mechanism of MscL

The mechanosensitive channel of large conductance, which serves as a model system for mechanosensitive channels, has previously been crystallized in the closed form, but not in the open form. Ensemble measurements and electrophysiological sieving experiments show that the open-diameter of the channel pore is >25Å, but the exact size and whether the conformational change follows a helix-tilt or barrel-stave model are unclear. Here we report measurements of the distance changes on liposome-reconstituted MscL transmembrane α-helices, using a "virtual sorting" single-molecule fluorescence energy transfer. We observed directly that the channel opens via the helix-tilt model and the open pore reaches 2.8 nm in diameter. In addition, based on the measurements, we developed a molecular dynamics model of the channel structure in the open state which confirms our direct observations.

q-bio.BM↗