TY - JOUR
T1 - The interaction dynamics of a negative feedback loop regulates flagellar number in Salmonella enterica serovar Typhimurium
AU - Aldridge, Christine
AU - Poonchareon, Kritchai
AU - Saini, Supreet
AU - Ewen, Thomas
AU - Soloyva, Alexandra
AU - Rao, Christopher V.
AU - Imada, Katsumi
AU - Minamino, Tohru
AU - Aldridge, Phillip D.
PY - 2010/12
Y1 - 2010/12
N2 - Each Salmonella enterica serovar Typhimurium cell produces a discrete number of complete flagella. Flagellar assembly responds to changes in growth rates through FlhD4C2 activity. FlhD4C2 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 σ28 activity. We have found that efficient growth-dependent regulation of FlhD4C2 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 FlhD4C2 activity. To investigate why, we characterized the biochemical interactions in the FliT FliD FlhD4C2 circuit. When FlhD4C2 was not bound to DNA, FliT disrupted the FlhD4C2 complex. Interestingly, when FlhD4C2 was bound to DNA it was insensitive to FliT regulation. This suggests that the FliT circuit regulates FlhD4C2 activity by preventing the formation of the FlhD4C2:DNA complex. Our data would suggest that this level of endogenous regulation of FlhD4C2 activity allows the flagellar system to efficiently respond to external signals.
AB - Each Salmonella enterica serovar Typhimurium cell produces a discrete number of complete flagella. Flagellar assembly responds to changes in growth rates through FlhD4C2 activity. FlhD4C2 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 σ28 activity. We have found that efficient growth-dependent regulation of FlhD4C2 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 FlhD4C2 activity. To investigate why, we characterized the biochemical interactions in the FliT FliD FlhD4C2 circuit. When FlhD4C2 was not bound to DNA, FliT disrupted the FlhD4C2 complex. Interestingly, when FlhD4C2 was bound to DNA it was insensitive to FliT regulation. This suggests that the FliT circuit regulates FlhD4C2 activity by preventing the formation of the FlhD4C2:DNA complex. Our data would suggest that this level of endogenous regulation of FlhD4C2 activity allows the flagellar system to efficiently respond to external signals.
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U2 - 10.1111/j.1365-2958.2010.07415.x
DO - 10.1111/j.1365-2958.2010.07415.x
M3 - Article
C2 - 21143315
AN - SCOPUS:78649658125
VL - 78
SP - 1416
EP - 1430
JO - Molecular Microbiology
JF - Molecular Microbiology
SN - 0950-382X
IS - 6
ER -