This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rosu, V. Articles by Hughes, K. T. Search for Related Content PubMed PubMed Citation Articles by Rosu, V. Articles by Hughes, K. T.

Translation Inhibition of the Salmonella fliC Gene by the fliC 5' Untranslated Region, fliC Coding Sequences, and FlgM

Department of Microbiology, Box 357242, University of Washington, Seattle, Washington 98195,¹ Department of Biology, University of Utah, Salt Lake City, Utah 84112²

Received 12 October 2005/ Accepted 24 March 2006

The 5'-untranslated region (5'UTR) of the fliC flagellin gene of Salmonella contains sequences critical for efficient fliC mRNA translation coupled to assembly. In a previous study we used targeted mutagenesis of the 5' end of the fliC gene to isolate single base changes defective in fliC gene translation. This identified a predicted stem-loop structure, SL2, as an effector of normal fliC mRNA translation. A single base change (–38C:U) in the fliC 5'UTR resulted in a mutant that is defective in fliC mRNA translation and was chosen for this study. Motile (Mot⁺) revertants of the –38C:T mutant were isolated and characterized, yielding several unexpected results. Second-site suppressors that restored fliC translation and motility included mutations that disrupt a RNA duplex stem formed between RNA sequences in the fliC 5'UTR SL2 region (including a precise deletion of SL2) and bases early within the fliC-coding region. A stop codon mutation at position 80 of flgM also suppressed the –38C:T motility defect, while flgM mutants defective in anti-²⁸ activity had no effect on fliC translation. One remarkable mutation in the fliC 5'UTR (–15G:A) results in a translation defect by itself but, in combination with the –38C:U mutation, restores normal translation. These results suggests signals intrinsic to the fliC mRNA that have both positive and negative effects on fliC translation involving both RNA structure and interacting proteins.

This article has been cited by other articles:

• Zhao, K., Liu, M., Burgess, R. R. (2007). Adaptation in bacterial flagellar and motility systems: from regulon members to 'foraging'-like behavior in E. coli. Nucleic Acids Res 35: 4441-4452 [Abstract] [Full Text]  
• Haugen, B. J., Pellett, S., Redford, P., Hamilton, H. L., Roesch, P. L., Welch, R. A. (2007). In Vivo Gene Expression Analysis Identifies Genes Required for Enhanced Colonization of the Mouse Urinary Tract by Uropathogenic Escherichia coli Strain CFT073 dsdA. Infect. Immun. 75: 278-289 [Abstract] [Full Text]