Evidence for interactions between MotA and MotB, torque-generating elements of the flagellar motor of Escherichia coli.

摘要: Abstract Cells that overexpress MotA (encoded on a plasmid derived from pBR322) grow slowly because of proton leakage. We have traced this defect to the coexpression fusion protein consisting 60 amino acids N terminus MotB and 50 specified by pBR322. Mutations within terminus, known abolish function when present in full-length MotB, reversed growth defect. Growth also was normal coexpressed with wild-type or series N-terminal fragments.