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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: Mol Microbiol. 2010 Dec 7;79(3):686–699. doi: 10.1111/j.1365-2958.2010.07477.x

FIG. 7.

FIG. 7

Summary of Aer-2 deletions and the steady-state behavior mediated by these fragments in E. coli BT3388. Cells expressing WT Aer-2 (res. 1–679) or the Δ1–37 Aer-2 mutant tumbled in air and swam smoothly (<1% tumbling) in N2 (in the absence of a diatomic oxy-gas). Removing the N-terminal HAMP 2 and/or HAMP 3 domains resulted in a locked kinase-off phenotype, whereas removing C-terminal HAMP 4 and/or HAMP 5 resulted in a kinase-on phenotype. The default state of the isolated kinase control module was on, but it reverted to a kinase-off state in the presence of HAMP 5 or HAMP 4 and 5. All cells were induced with 200 µM IPTG for 45 min before monitoring their swimming behavior in a gas perfusion chamber. Mutants exhibiting less than 1% tumbling in air showed the same response after induction with 1 mM IPTG. Abbreviation: H, HAMP.