HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (Papers in Press[PDF]) All Versions of this Article: mic.0.026294-0v1 155/6/1890    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ding, L. Articles by Chen, S. Search for Related Content PubMed PubMed Citation Articles by Ding, L. Articles by Chen, S. Agricola Articles by Ding, L. Articles by Chen, S.

Functional characterization of FlgM in the regulation of flagellar synthesis and motility in Yersinia pseudotuberculosis

¹ Wuhan Institute of Virology, The Chinese Academy of Sciences;
² Institute of Infection, Immunity and Inflammation, University of Nottingham;
³ University of Nottingham;
⁴ Wuhan Institute of Virology, the Chinese Academy of Sciences

ABSTRACT

We describe here the functional characterization of the flgM gene in Yersinia pseudotuberculosis. Direct interaction of FlgM with the alternative sigma factor 28 (FliA) was first confirmed. A conserved region in the C-terminus of FlgM was found which included the 28 binding domain. By site-directed mutagenesis, bacterial two-hybrid and Western blotting, the primary FlgM binding sites with 28 were shown to be Ile85, Ala86 and Leu89. A role for FlgM in swimming motility was demonstrated by inactivation of flgM and subsequent complementation in trans. Transcriptional fusion analyses showed differential gene expression of flhDC, fliA, flgM and fliC in the fliA and flgM mutants compared with the wild-type. flhDC expression was not influenced by 28 or FlgM while fliA expression was abolished in the fliA mutant and considerably reduced in the flgM mutant when compared to the wild type indicating both FliA and FlgM can activate fliA transcription. Conversely flgM transcription was higher in the fliA mutant when compared to the wild type, suggesting that flgM transcription was repressed by 28. Interestingly, fliC expression was markedly increased in the flgM mutant, suggesting a negative regulatory role for FlgM on fliC expression. The transcription of other -dependent genes (cheW, flgD, flaA, csrA and fliZ) was also examined in fliA and flgM mutant backgrounds and revealed that other -factors apart from 28 may be involved in flagella biogenesis in Y. pseudotuberculosis. When the motility phenotypes and consequences of flgM mutation on the regulation of these key motility genes are taken together we propose that the mechanisms regulating flagella biogenesis in Y. pseudotuberculosis may differ from those described for other bacteria.

⁵ E-mail: sychen{at}wh.iov.cn

This article has been cited by other articles:

				Y. Hu, Y. Wang, L. Ding, P. Lu, S. Atkinson, and S. Chen Positive regulation of flhDC expression by OmpR in Yersinia pseudotuberculosis Microbiology, November 1, 2009; 155(11): 3622 - 3631. [Abstract] [Full Text] [PDF]