E. Kitamura, Y. Nakayama, H. Matsuzaki
Dec 23, 1994
Bioscience, biotechnology, and biochemistry
The Escherichia coli pgsA3 mutation, which causes acidic-phospholipid deficiency, was found to repress the flagellar master operon, as assessed by the beta-galactosidase activities of flhD-lacZ fusions. This explained the impairment of flagellar formation and motility by the mutation. A series of deletion analysis indicated that a 40-bp region, at the 5' end of the flhD locus examined, was responsible for the repression of a downstream transcription initiation that was catabolite-repression sensitive. This novel regulatory region was 200 bp upstream of the first possible translation initiation site.