The interaction dynamics of a negative feedback loop regulates flagellar number in Salmonella enterica serovar Typhimurium

被引：35

作者：

Aldridge, Christine ^{[1
,2
]}

Poonchareon, Kritchai ^{[1
,2
]}

Saini, Supreet ^{[3
]}

Ewen, Thomas ^{[1
,2
]}

Soloyva, Alexandra ^{[2
]}

Rao, Christopher V. ^{[3
]}

Imada, Katsumi ^{[4
]}

Minamino, Tohru ^{[4
,5
]}

Aldridge, Phillip D. ^{[1
,2
]}

机构：

[1] Newcastle Univ, Ctr Bacterial Cell Biol, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England

[2] Newcastle Univ, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England

[3] Univ Illinois, Dept Chem & Biomol Engn, Urbana, IL USA

[4] Osaka Univ, Grad Sch Frontier Biosci, Osaka, Japan

[5] JST, PRESTO, Kawaguchi, Saitama, Japan

来源：

MOLECULAR MICROBIOLOGY | 2010年 / 78卷 / 06期

基金：

英国生物技术与生命科学研究理事会; 美国国家科学基金会;

关键词：

III SECRETION CHAPERONE; ESCHERICHIA-COLI; TRANSCRIPTIONAL CONTROL; MASTER REGULATOR; PROTEIN; REGULON; FLIT; FLGM; BINDING; GENES;

D O I：

10.1111/j.1365-2958.2010.07415.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：1416 / 1430

页数：15

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