Search arXiv⌕ Search
Home/Archive/arXiv

arXiv · 2007.13368

Recent Advances and Prospects in the Research of Nascent Adhesions

Henning Stumpf·Andreja Ambriović-Ristov·Aleksandra Radenovic·Ana-Sunčana Smith
View original source ↗Read source document ↗Export metadata ↓

Abstract

Nascent adhesions are submicron transient structures promoting the early adhesion of cells to the extracellular matrix. Nascent adhesions typically consist of several tens of integrins, and serve as platforms for the recruitment and activation of proteins to build mature focal adhesions. They are also associated with early stage signalling and the mechanoresponse. Despite their crucial role in sampling the local extracellular matrix, very little is known about the mechanism of their formation. Consequently, there is a strong scientific activity focused on elucidating the physical and biochemical foundation of their development and function. Precisely the results of this effort will be summarized in this article.

Explore related subjects

q-bio.SCphysics.bio-ph

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Henning Stumpf, Andreja Ambriović-Ristov, Aleksandra Radenovic, Ana-Sunčana Smith. 2020-07-27. Recent Advances and Prospects in the Research of Nascent Adhesions. https://doi.org/10.3389/fphys.2020.574371

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related papers

arXiv2026

Clustering versus sorting: a mass-conserving reaction-diffusion model of planar polarity puncta

Planar cell polarity is preceded by the clustering of polarity proteins into discrete, low-turnover membrane subdomains (puncta), yet the minimal interactions that nucleate puncta, set their number, and segregate opposite orientations remain unclear. We address these questions with a mass-conserving reaction-diffusion model in which two diffusible monomers bind reversibly across a cell-cell junction into trans-complexes of two orientations, with feedback entering only through concentration-dependent rates. Above a critical density, the uniform state undergoes a long-wavelength mass-redistribution instability rather than a finite-wavelength Turing bifurcation. The form of the feedback then selects between two morphologies: broad mesas fixed by a Maxwell construction under saturating feedback, and narrow mass-limited spikes under unbounded feedback. For spikes we obtain closed-form expressions exhibiting a clean separation of amplitude (mass and feedback), width (the complex diffusion length), and spacing (the monomer screening length). Within a fast-monomer reduction we prove, for any number and arrangement of puncta, that like-oriented arrays coarsen, so multiplicity is metastable and kinetically determined. The second monomer reservoir introduces a second screening length that rate-limits competition by the harmonic mean of the monomer diffusivities, and the spectrum of a punctum remains free of oscillatory ("blinking") instabilities throughout. Finally, sign-definite cross-modulation of turnover converts clustering into orientation sorting - the mutual exclusion of orientations along a single contact: mass redistribution sets puncta number, and the sign of the cross-coupling determines whether orientations segregate. Puncta number and orientation sorting are thus governed by mathematically separable ingredients.

q-bio.SC↗
arXiv2026

Distributed delay stabilizes bistable genetic networks

Delay is an inherent feature of genetic regulatory networks. It represents the time required for the assembly of functional regulator proteins. The protein production process is complex, as it includes transcription, translocation, translation, folding, and oligomerization. Because these steps are noisy, the resulting delay associated with protein production is distributed (random). We here consider how distributed delay impacts the dynamics of bistable genetic circuits. We show that for a variety of genetic circuits that exhibit bistability, increasing the noise level in the delay distribution dramatically stabilizes the metastable states. By this we mean that mean residence times in the metastable states dramatically increase. Relevance to Life Sciences. Bistable genetic regulatory networks are ubiquitous in living organisms. Evolutionary processes seem to have tuned such networks so that they switch between metastable states when it is important to do so, but small fluctuations do not cause unwanted switching. Understanding how evolution has tuned the stability of biological switches is an important problem. In particular, such understanding can guide the design of forward-engineered synthetic bistable genetic regulatory networks. Mathematical Content. We use two methods to explain this stabilization phenomenon. First, we introduce and simulate stochastic hybrid models that depend on a switching-rate parameter. These stochastic hybrid models allow us to unfold the distributed-delay models in the sense that, in certain cases, the distributed-delay model can be viewed as a fast-switching limit of the corresponding stochastic hybrid model. Second, we generalize the three-states model, a symbolic model of bistability, and analyze this extension.

q-bio.SC↗
arXiv2026

The role of estrogen receptor alpha on calcium transport during smooth muscle contractions

Reproductive hormones regulate a wide range of physiological processes throughout the human lifespan. Estrogen, in particular, varies substantially across the menstrual cycle and is widely used in contraceptives and hormone replacement therapies. Despite its physiological importance, few experimental studies and even fewer mathematical models explicitly investigate how estrogen regulates smooth muscle function. As smooth muscle lines our blood vessels, airways, uterus, and several other organs, understanding how estrogen impacts smooth muscle is important to improving the understanding of sex differences in lifelong health. Here we extend an established mathematical model of smooth muscle cell calcium signalling to incorporate estrogen-dependent modulation of intracellular calcium transport pathways. Numerical simulations, global sensitivity analysis, and numerical bifurcation analysis are then used to quantify the influence of estrogen on intracellular calcium dynamics and the resulting steady-state and oscillatory behaviours. Our results demonstrate that physiologically relevant changes in estrogen shift intracellular calcium concentrations while leaving the underlying bifurcation structure and qualitative dynamics largely unchanged, suggesting that estrogen acts primarily as a quantitative modulator of smooth muscle calcium signalling. This work also serves to establish a foundation for future mechanistic models of hormone-dependent cell physiology.

q-bio.SC↗