Salmonella typhimurium mutants generally defective in chemotaxis.

The mutations of eight chemotaxis-deficient strains of Salmonella typhimurium, including five new mutants in strain LT2, were mapped by P22 transduction in relation to various fla mot deletions in S. abortus-equi. Seven recessive che mutations mapped between motB and flaC: three, all nontumbling, the che region I, adjacent to motB, and four, including one ever-tumbling, in che region II, adjacent to flaC. Mutant che-107, never-tumbling and dominant to wild type, mapped at flaAII, other mutations of which cause either absence of flagella or lack of locomotor function. We surmise that gene flaAII specifies a protein that polymerizes to form an essential component of the basal apparatus (so that absence of gene product prevents formation of flagela); that a component built up from certain mutationally altered proteins cannot transmit (or generate) active rotation of the hook and flagellum, and so causes the Mot (paralysis) phenyotype; and that a component built up from protein with the che-107 alteration permits only counterclockwise rotation, so that the tumble, normally produced by transient clockwise rotation, cannot be effected.