Turing-pattern model of scaffolding proteins that establish spatial asymmetry during the cell cycle of Caulobacter crescentus

The crescent-shaped bacterium Caulobacter crescentus divides asymmetrically into a sessile (stalked) cell and a motile (flagellated) cell. This dimorphic cell division cycle is driven by the asymmetric appearance of scaffolding proteins at the cell's stalk and flagellum poles. The scaffolding proteins recruit enzyme complexes that phosphorylate and degrade a master transcription factor, CtrA, and the abundance and phosphorylation state of CtrA control the onset of DNA synthesis and the differentiation of stalked and flagellated cell types. In this study, we use a Turing-pattern mechanism to simulate the spatiotemporal dynamics of scaffolding proteins in Caulobacter and how they influence the abundance and intracellular distribution of CtrA similar to P. Our mathematical model captures crucial features of wild-type and mutant strains and predicts the distributions of CtrA similar to P and signaling proteins in mutant strains. Our model accounts for Caulobacter polar morphogenesis and shows how spatial localization and phosphosignaling cooperate to establish asymmetry during the cell cycle.

Automated summary

The bacterium Caulobacter crescentus undergoes an asymmetric division into a stalked cell and a flagellated cell. This asymmetry is driven by the appearance of scaffolding proteins that recruit enzyme complexes to regulate the transcription factor CtrA. Our study uses a Turing-pattern mechanism to simulate the dynamics of these scaffolding proteins and their influence on CtrA abundance and distribution. The mathematical model captures key features of wild-type and mutant strains and predicts the distributions of CtrA and signaling proteins in mutants, providing insights into polar morphogenesis and asymmetry during the cell cycle in Caulobacter.