Affiliation:
1. Department of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801
Abstract
ABSTRACT
Type I fimbriae in
Salmonella enterica
serovar Typhimurium are surface appendages that facilitate binding to eukaryotic cells. Expression of the
fim
gene cluster is known to be regulated by three proteins—FimW, FimY, and FimZ—and a tRNA encoded by
fimU
. In this work, we investigated how these proteins and tRNA coordinately regulate
fim
gene expression. Our results indicate that FimY and FimZ independently activate the P
fimA
promoter which controls the expression of the
fim
structural genes. FimY and FimZ were also found to strongly activate each other's expression and weakly activate their own expression. FimW was found to negatively regulate
fim
gene expression by repressing transcription from the P
fimY
promoter, independent of FimY or FimZ. Moreover, FimW and FimY interact within a negative feedback loop, as FimY was found to activate the P
fimW
promoter. In the case of
fimU
, the expression of this gene was not found to be regulated by FimW, FimY, or FimZ. We also explored the effect of
fim
gene expression on
Salmonella
pathogenicity island 1 (SPI1). Our results indicate that FimZ alone is able to enhance the expression of
hilE
, a known repressor of SPI1 gene expression. Based on our results, we were able to propose an integrated model for the
fim
gene circuit. As this model involves a combination of positive and negative feedback, we hypothesized that the response of this circuit may be bistable and thus a possible mechanism for phase variation. However, we found that the response was continuous and not bistable.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
57 articles.
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