Theory of Active Intracellular Transport by DNA-relaying

TL;DR

This paper develops a minimal theoretical model to describe how DNA elasticity and ParA gradients facilitate active chromosome segregation in bacteria, revealing four distinct force-generation regimes.

Contribution

It introduces a novel minimal model capturing the DNA-relay mechanism for force generation in bacterial chromosome segregation.

Findings

Identifies four distinct force-generation regimes based on chromosome fluctuations.

Shows interplay between ParA gradient, chromosome elasticity, and friction forces.

Provides a mechanistic framework for understanding active intracellular transport.

Abstract

The spatiotemporal organization of bacterial cells is crucial for the active segregation of replicating chromosomes. In several species, including Caulobacter crescentus, the ATPase ParA binds to DNA and forms a gradient along the long cell axis. The ParB partitioning complex on the newly replicated chromosome translocates up this ParA gradient, thereby contributing to chromosome segregation. A DNA-relay mechanism - deriving from the elasticity of the fluctuating chromosome - has been proposed as the driving force for this cargo translocation, but a mechanistic theoretical description remains elusive. Here, we propose a minimal model to describe force generation by the DNA-relay mechanism over a broad range of operational conditions. Conceptually, we identify four distinct force-generation regimes characterized by their dependence on chromosome fluctuations. These relay force regimes arise from an interplay of the imposed ParA gradient, chromosome fluctuations, and an emergent friction force due chromosome-cargo interactions.