Modeling partitioning of Min proteins between daughter cells after septation in Escherichia coli

TL;DR

This study investigates how Min proteins are unevenly partitioned between daughter cells in E. coli after septation, affecting their oscillation behavior, using a detailed 3D model to identify causes and potential biological solutions.

Contribution

The paper analyzes the septation process in a 3D Min protein model to identify causes of asymmetric partitioning and suggests biological mechanisms to reduce partitioning errors.

Findings

Up to 85% of daughter cells oscillate after septation.

Partitioning issues occur at specific MinD and MinE oscillation phases.

Enhanced MinD binding does not significantly improve oscillation in daughter cells.

Abstract

Ongoing sub-cellular oscillation of Min proteins is required to block minicelling in E. coli. Experimentally, Min oscillations are seen in newly divided cells and no minicells are produced. In model Min systems many daughter cells do not oscillate following septation because of unequal partitioning of Min proteins between the daughter cells. Using the 3D model of Huang et al., we investigate the septation process in detail to determine the cause of the asymmetric partitioning of Min proteins between daughter cells. We find that this partitioning problem arises at certain phases of the MinD and MinE oscillations with respect to septal closure and it persists independently of parameter variation. At most 85% of the daughter cells exhibit Min oscillation following septation. Enhanced MinD binding at the static polar and dynamic septal regions, consistent with cardiolipin domains, does not substantially increase this fraction of oscillating daughters. We believe that this problem will be shared among all existing Min models and discuss possible biological mechanisms that may minimize partitioning errors of Min proteins following septation.