On the length scale dependence of DNA conformational change under local perturbation

Soumyadip Banerjee; Kushal Shah; Shaunak Sen

Home/Archive/arXiv

arXiv · 1911.04711

On the length scale dependence of DNA conformational change under local perturbation

Soumyadip Banerjee·Kushal Shah·Shaunak Sen

View original source ↗Read source document ↗Export metadata ↓

Abstract

Conformational change of a DNA molecule is frequently observed in multiple biological processes and has been modelled using a chain of strongly coupled oscillators with a nonlinear bistable potential. While the mechanism and properties of conformational change in the model have been investigated and several reduced order models developed, the conformational dynamics as a function of the length of the oscillator chain is relatively less clear. To address this, we used a modified Lindstedt-Poincare method and numerical computations. We calculate a perturbation expansion of the frequency of the model's nonzero modes, finding that approximating these modes with their unperturbed dynamics, as in a previous reduced order model, may not hold when the length of the DNA model increases. We investigate the conformational change to local perturbation in models of varying lengths, finding that for chosen input and parameters, there are two regions of DNA length in the model, first where the minimum energy required to undergo the conformational change increases with DNA length; and second, where it is almost independent of the length of the DNA model. We analyze the conformational change in these models by adding randomness to the local perturbation, finding that the tendency of the system to remain in a stable conformation against random perturbation decreases with an increase in the DNA length. These results should help to understand the role of the length of a DNA molecule in influencing its conformational dynamics.

Explore related subjects

physics.bio-ph cond-mat.soft q-bio.BM

Keep this discovery

BibTeX RIS

Soumyadip Banerjee, Kushal Shah, Shaunak Sen. 2019-11-12. On the length scale dependence of DNA conformational change under local perturbation. https://arxiv.org/abs/1911.04711

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

KEEP EXPLORING

Related papers

arXiv2026

Multiscale retinal flow on a spherical cap of varying aperture

Modelling retinal haemodynamics is crucial for understanding retinal microcirculation but is computationally demanding because it involves coupling between the vasculature and surrounding tissue across multiple scales. This computational burden has been substantially alleviated by a recent analytic solution on the planar disc that enables lumping the capillary bed and surrounding tissue into an effective resistor. However, that formulation treats the retina as a flat surface, whereas the retina is a curved surface with a finite anterior aperture. In this work, we develop a nontrivial and physiologically necessary extension to spherical-cap tissue domains with varying apertures, where surface curvature and finite-aperture boundaries complicate solving coupled Darcy equations on a curved manifold. Using a stereographic projection and a decoupling transformation, we derive an analytic solution for the capillary-tissue system on the spherical cap that represents flow in both the capillary bed and interstitial tissue more realistically while retaining the efficient resistor formulation, a key advantage of the planar-disc formulation. This solution is coupled to one-dimensional (1D) arteriolar and venular flows to obtain a multiscale description of retinal haemodynamics. Using a vasculature model designed to capture retinal vascular features, we show that the multiscale model's predictions are consistent with experimental data. We further explore aperture effects using both a fixed hemispherical vasculature and aperture-dependent vasculature. The aperture affects retinal haemodynamics mainly through changes in the constructed vasculature itself, whereas the surface-averaged pressures and relative terminal flow distributions remain nearly unchanged. This framework provides a foundation for studying retinal pathophysiology on more anatomically realistic domains.

physics.bio-ph↗

arXiv2026

Double-well potentials and crucial estimations in nonlinear dynamics of microtubules

In the present work, we study the two-component model of microtubules, the basic components of the eukaryotic cytoskeleton. We introduce a couple of estimations, which tremendously simplified the model. The paper is devoted to tangential oscillations of dimers, but we explain that the model can explain the radial oscillations as well. Finally, we study the stability of all solutions of differential equations, describing the dynamics of the microtubules.

physics.bio-ph↗

arXiv2026

A thermodynamically consistent framework for finite growth of multi-constituent mixtures with application to tumor growth

Biological tissues grow by continuously producing, transporting, and reorganizing multiple interacting constituents. These processes are intrinsically coupled to finite deformation and residual stress. Existing models typically capture either finite growth kinematics or multi-constituent transport, but rarely both within a thermodynamically consistent setting. In particular, existing approaches do not consistently link the volume created by finite growth to the mass produced for each individual constituent. In this work, we develop a general continuum framework that unifies finite growth kinematics and multiphase mixture theory for fully saturated multi-constituent mixtures containing an arbitrary number of dilute dissolved solutes. Formulated in a solid-skeleton-based description, the framework rests on constituent-wise balance laws and a free-energy dissipation principle, from which thermodynamically admissible constitutive closures are derived for all mass-exchange, transport, reaction, and growth processes. The central novelty of the framework is a coupling between growth-induced volume creation and constituent mass production, expressed through volume accumulation fractions that distribute the newly created volume among the constituents while preserving saturation. We cast the resulting model in a total Lagrangian mixed weak form and specialize the general theory to a four-constituent, two-solute model of avascular tumor growth that couples nutrient transport, waste production, phenotype transitions between proliferative, hypoxic, and necrotic cells, volume growth, elastic deformation, and growth-induced residual stress. The model is implemented within a finite element setting and its capabilities are demonstrated on representative benchmark problems.

physics.bio-ph↗