Simulated Clustering Dynamics of Colloidal Magnetic Nanoparticles

Magnetically guided self-assembly of nanoparticles is a promising bottom-up method to fabricate novel materials and superstructures, such as, for example, magnetic nanoparticle clusters for biomedical applications. The existence of assembled...

Collective Clustering Dynamics of SARS-COV-2 Particles

Collective spread of aggregated viral particles may have beneficial effects on viral capability to survive in the external environment, to counteract immune responses, and to successfully colonize host cells. Here we ask whether SARS-Cov-2 particles, responsible for COVID-19, display collective clustering behavior. Looking at microphotographs and movies of SARS-Cov-2 particles emerging from the surface of cultured cells, we describe single virions that tend to aggregate in progressively larger globular assemblies, until a network-like appearance is achieved. When SARS-Cov-2 particles stick into each other, the squeezing of single virions leads to improved viral package in host’s fluids. We discuss how these findings might explain both the ability to spread of SARS-Cov-2 and the clinical severity of COVID-19 in humans, paving the way to novel therapeutic strategies to mechanically disrupt collective clustering.

Nanoscale integrin cluster dynamics controls cellular mechanosensing via FAKY397 phosphorylation

Transduction of extracellular matrix mechanics affects cell migration, proliferation, and differentiation. While this mechanotransduction is known to depend on the regulation of focal adhesion kinase phosphorylation on Y397 (FAKpY397), the mechanism remains elusive. To address this, we developed a mathematical model to test the hypothesis that FAKpY397-based mechanosensing arises from the dynamics of nanoscale integrin clustering, stiffness-dependent disassembly of integrin clusters, and FAKY397 phosphorylation within integrin clusters. Modeling results predicted that integrin clustering dynamics governs how cells convert substrate stiffness to FAKpY397, and hence governs how different cell types transduce mechanical signals. Existing experiments on MDCK cells and HT1080 cells, as well as our new experiments on 3T3 fibroblasts, confirmed our predictions and supported our model. Our results suggest a new pathway by which integrin clusters enable cells to calibrate responses to their mechanical microenvironment.