Journal
MOLECULAR MICROBIOLOGY
Volume 78, Issue 6, Pages 1416-1430Publisher
WILEY
DOI: 10.1111/j.1365-2958.2010.07415.x
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Funding
- BBSRC [BB/D015855/1]
- Nareasuan University (Thailand)
- National Science Foundation [CBET 0644744]
- Public Health Service [GM083601, GM054365]
- Ministry of Education, Science and Culture of Japan
- Diawa Foundation
- Royal Society (UK)
- Biotechnology and Biological Sciences Research Council [BB/D015855/1] Funding Source: researchfish
- BBSRC [BB/D015855/1] Funding Source: UKRI
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P>Each Salmonella enterica serovar Typhimurium cell produces a discrete number of complete flagella. Flagellar assembly responds to changes in growth rates through FlhD(4)C(2) activity. FlhD(4)C(2) activity is negatively regulated by the type 3 secretion chaperone FliT. FliT is known to interact with the flagellar filament cap protein FliD as well as components of the flagellar type 3 secretion apparatus. FliD is proposed to act as an anti-regulator, in a manner similar to FlgM inhibition of sigma 28 activity. We have found that efficient growth-dependent regulation of FlhD(4)C(2) requires FliT regulation. In turn, FliD regulation of FliT modulates the response. We also show that, unlike other flagellar-specific regulatory circuits, deletion of fliT or fliD did not lead to an all-or-nothing response in FlhD(4)C(2) activity. To investigate why, we characterized the biochemical interactions in the FliT : FliD : FlhD(4)C(2) circuit. When FlhD(4)C(2) was not bound to DNA, FliT disrupted the FlhD(4)C(2) complex. Interestingly, when FlhD(4)C(2) was bound to DNA it was insensitive to FliT regulation. This suggests that the FliT circuit regulates FlhD(4)C(2) activity by preventing the formation of the FlhD(4)C(2):DNA complex. Our data would suggest that this level of endogenous regulation of FlhD(4)C(2) activity allows the flagellar system to efficiently respond to external signals.
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