摘要
Recent extensive studies of Escherichia coli （E. coli） chemotaxis have achieved a deep understanding of its mi- croscopic control dynamics. As a result, various quantitatively predictive models have been developed to describe the chemotactic behavior of E. coli motion. However, a population-level partial differential equation （PDE） that rationally incorporates such microscopic dynamics is still insufficient. Apart from the traditional Keller-Segel （K-S） equation, many existing population-level models developed from the microscopic dynamics are integro-PDEs. The difficulty comes mainly from cell tumbles which yield a velocity jumping process. Here, we propose a Langevin approximation method that avoids such a difficulty without appreciable loss of precision. The resulting model not only quantitatively repro- duces the results of pathway-based single-cell simulators, but also provides new inside information on the mechanism of E. coli chemotaxis. Our study demonstrates a possible alternative in establishing a simple population-level model that allows for the complex microscopic mechanisms in bacterial chemotaxis.
Recent extensive studies of Escherichia coli （E. coli） chemotaxis have achieved a deep understanding of its mi- croscopic control dynamics. As a result, various quantitatively predictive models have been developed to describe the chemotactic behavior of E. coli motion. However, a population-level partial differential equation （PDE） that rationally incorporates such microscopic dynamics is still insufficient. Apart from the traditional Keller-Segel （K-S） equation, many existing population-level models developed from the microscopic dynamics are integro-PDEs. The difficulty comes mainly from cell tumbles which yield a velocity jumping process. Here, we propose a Langevin approximation method that avoids such a difficulty without appreciable loss of precision. The resulting model not only quantitatively repro- duces the results of pathway-based single-cell simulators, but also provides new inside information on the mechanism of E. coli chemotaxis. Our study demonstrates a possible alternative in establishing a simple population-level model that allows for the complex microscopic mechanisms in bacterial chemotaxis.
