Optimal Mutation Rates on Static Fitness Landscpes

M. Nilsson

Home/Archive/arXiv

arXiv · physics/0005018

Optimal Mutation Rates on Static Fitness Landscpes

M. Nilsson

View original source ↗Read source document ↗Export metadata ↓

Abstract

We study the evolution of mutation rates for an asexual population living on a static fitness landscape, consisting of multiple peaks forming an evolutionary staircase. The optimal mutation rate is found by maximizing the diffusion towards higher fitness. Surprisingly the optimal genomic copying fidelity is given by Q = e^(-1/ln(n)) (where n is the genome length), independent of all other parameters in the model. Simulations confirm this theoretical result. We also discuss the relation between the optimal mutation rate on static and dynamic fitness landscapes.

Explore related subjects

physics.bio-ph q-bio

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

M. Nilsson. 2000-05-08. Optimal Mutation Rates on Static Fitness Landscpes. https://arxiv.org/abs/physics/0005018

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

KEEP EXPLORING

Related papers

arXiv2026

Inferring cell property distributions from high-throughput measurement data with cell-to-cell variability

High-throughput measurements of cell populations produce broad distributions of observables due to inherent cell-to-cell variability. While these distributions contain valuable biological information, extracting the underlying distributions of cellular properties remains challenging. We introduce the likelihood functional, a statistical framework that infers cell property distributions by combining experimental data with deterministic computational models. The method first evaluates the model on a discrete parameter grid. Optimization of the likelihood functional is then possible without repeated model evaluations and yields best-fit property distributions which enable the direct prediction of observable distributions for comparison with experiments. As a demonstration, we apply the framework to real-time deformability cytometry data and infer cytosol and membrane viscosity distributions of human red blood cells.

physics.bio-ph↗

arXiv2026

Hyaluronic acid over-expression drives tissue architecture in both healthy and diseased states

Tissue architecture is shaped by a variety of biomechanical and biochemical mechanisms, including morphogen patterning, differential growth, and spatial variations in cellular contractility. These mechanisms typically emphasize forces generated within cells. Here, we explore a complementary mechanism in which intercellular space itself exerts forces that shape tissue architecture. More specifically, we focus on hyaluronic acid (HA), a glycosaminoglycan of the extracellular matrix, that draws fluid into the spaces between cells through osmotic pressure, allowing these spaces to expand and mechanically deform the surrounding tissue. We propose that spatial patterning of HA-mediated extracellular forces, acting together with tissue geometry and junctional mechanics, provides a common physical framework capable of generating distinct tissue architectures. We test this hypothesis using a computational framework coupling a cell-based extended vertex model for biological tissues to a flow network representing HA and extracellular fluid in the extracellular space. This coupled model demonstrates a range of architectural responses spanning changes in tissue topology and morphology: global HA overexpression drives fluid accumulation and cell-cell junction rupture to produce multiple lumens in nontrivial patterns; a localized HA-rich region generates pressure gradients that drive budding; {\it multiple localized HA-rich regions generate branching;} and {\it extended HA-rich patterns can drive tubular structures.} Our results have direct experimental implications and establish the spatial patterning of HA-mediated intercellular forces as a mechanical morphogen helping shape tissue architecture.

physics.bio-ph↗

arXiv2026

Spontaneous Mutations from Terahertz Proton Tunneling

Protons in the bonds between base pairs of the double helix store the code of life by breaking the dyad symmetry that swaps the sense strand with its complementary partner. When these bonds break during replication and transcription, pairs of protons switch sides, restoring dyad symmetry and destroying genetic information. The observed rate of such spontaneous mutations is obtained in the sudden approximation for bond breaking provided protons in bonds between bases tunnel across the gap with terahertz frequency.

physics.bio-ph↗