Stolz B, Berg H C
Department of Cellular, Harvard University, Cambridge, Massachusetts 02138.
J Bacteriol. 1991 Nov;173(21):7033-7. doi: 10.1128/jb.173.21.7033-7037.1991.
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 of a fusion protein consisting of 60 amino acids from the N terminus of MotB and 50 amino acids specified by pBR322. Mutations within the N terminus, known to abolish function when present in full-length MotB, reversed the growth defect. Growth also was normal when MotA was coexpressed with wild-type MotB or with a series of MotB N-terminal fragments.
过度表达MotA（由源自pBR322的质粒编码）的细胞由于质子泄漏而生长缓慢。我们已将此缺陷追溯至一种融合蛋白的共表达，该融合蛋白由MotB N端的60个氨基酸和pBR322指定的50个氨基酸组成。已知当存在于全长MotB中时会消除功能的N端内的突变，逆转了生长缺陷。当MotA与野生型MotB或一系列MotB N端片段共表达时，生长也正常。
