| Abstract: | The genetic relationship between tsr and cheD mutations, which affect chemotactic ability and map at approximately 99 min on the Escherichia coli chromosome, was investigated. Mutants defective in tsr function typically exhibited wild-type swimming patterns, but were unable to carry out chemotactic responses to a number of attractant and repellent chemicals. In contrast, cheD mutants swam smoothly, with few spontaneous directional changes, and were generally nonchemotactic. In complementation tests, cheD mutations, unlike tsr, proved to be dominant to wild type, suggesting that the cheD defect might be due to an active inhibitor of chemotaxis. Mutations that inactivated the putative inhibitor were obtained by selecting for restoration of chemotactic ability or for loss of cheD dominance. The resultant double mutants were shown to carry the original cheD mutation and a second tightly linked mutation, some of which exhibited nonsense or temperature-sensitive phenotypes, implying that they had occurred in a structural gene for a protein. All such double mutants behaved like typical tsr mutants in all other respects, including complementation pattern, swimming behavior, and chemotactic ability. These findings implied that either overproduction of tsr product or synthesis of an aberrant tsr product was responsible for the chemotaxis defect of cheD strains. Such mutants should be useful in analyzing the role of the tsr product in chemotactic responses. |
