Abstract
Millions of people worldwide develop foodborne illnesses caused by Salmonella enterica (S. enterica) every year. The pathogenesis of S. enterica depends on flagella, which are appendages that the bacteria use to move through the environment. Interestingly, populations of genetically identical bacteria exhibit heterogeneity in the number of flagella. To understand this heterogeneity and the regulation of flagella quantity, we propose a mathematical model that connects the flagellar gene regulatory network to flagellar construction. A regulatory network involving more than 60 genes controls flagellar assembly. The most important member of the network is the master operon, flhDC, which encodes the FlhD4C2 protein. FlhD4C2 controls the construction of flagella by initiating the production of hook basal bodies (HBBs), protein structures that anchor the flagella to the bacterium. By connecting a model of FlhD4C2 regulation to a model of HBB construction, we investigate the roles of various feedback mechanisms. Analysis of our model suggests that a combination of regulatory mechanisms at the protein and transcriptional levels induce bistable FlhD4C2 levels and heterogeneous numbers of flagella. Also, the balance of regulatory mechanisms that become active following HBB construction is sufficient to provide a counting mechanism for controlling the total number of flagella produced.
Highlights
Millions of people worldwide develop foodborne illnesses caused by Salmonella enterica (S. enterica) every year [1]
We use mathematical models of the gene network that regulates flagellar construction to explore how the bacteria controls the number of flagella produced
The pathogenesis of S. enterica depends on flagella, which are appendages that the bacteria use to move through the environment
Summary
Millions of people worldwide develop foodborne illnesses caused by Salmonella enterica (S. enterica) every year [1]. Partridge and Harshey describes the distributions of the number of flagella per bacterium under different growth conditions [3] It was observed under each growth condition that some bacteria did not produce any flagella, while the number of flagella on bacteria that produced them roughly follows a normal distribution, where the mean depended on the growth condition. This phenotypic heterogeneity enables the evasion of the host immune system during acute infection [4]. It is not yet clear what mechanisms determine flagella heterogeneity and how the bacteria regulate the number of flagella produced
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