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PATHOGENICITY AND VIRULENCE |
1,3School and Graduate Institute of Medical Technology1 and Graduate Institute of Microbiology3, College of Medicine, National Taiwan University, 1 Jen Ai Road, 1st Section, Taipei, Taiwan, Republic of China 2Department of Laboratory Medicine, National Taiwan University Hospital, Taipei, Taiwan, Republic of China
Correspondence Won-Bo Wang wbwang{at}ha.mc.ntu.edu.tw
Received 11 July 2002 Accepted 12 August 2002
Swarming by Proteus mirabilis involves differentiation of typical short vegetative rods into filamentous hyper-flagellated swarm cells that undergo cycles of rapid and co-ordinated population migration across surfaces and exhibit high levels of virulence gene expression. RsmA (repressor of secondary metabolites) and CsrA, its homologue in Escherichia coli, control many phenotypic traits, such as motility and pathogenesis in Erwinia species, glycogen biosynthesis, cell size and biofilm formation in Escherichia coli and swarming motility in Serratia marcescens. To investigate the role of RsmA in Proteus mirabilis, the rsmA gene from Proteus mirabilis (hereafter referred to as rsmAPm) was cloned. RsmAPm showed high sequence similarity to Escherichia coli CsrA and RsmA cloned from Erwinia carotovora subsp. carotovora, Serratia marcescens, Haemophilus influenzae and Bacillus subtilis and could complement an Escherichia coli csrA mutant in glycogen synthesis. A low-copy-number plasmid carrying rsmAPm expressed from its native promoter caused suppression of swarming motility and expression of virulence factors in Proteus mirabilis. mRNA stability assays suggested that RsmAPm inhibited virulence factor expression through promoting mRNA degradation. RsmA homologues cloned from Serratia marcescens and Erwinia carotovora subsp. carotovora could also inhibit swarming and virulence factor expression in Proteus mirabilis.
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