Abstract
Three mutants with an autolysin-deficient and flagellaless phenotype (lyt) were genetically analyzed and compared with 3 thermosensitive flagellaless mutants. In view of the near indistinguishability of their phenotypes, all 6 mutantions were assigned to fla loci. They were distributed into 4 linkage groups, designated flaA-flaD. flaA and flaB map between pyrD and thyA, flaD maps between aroD and lys and, in agreement with a previous report, flaC maps near his-A. A locus associated with hypermotility, ifm-3, maps near the latter marker. Introduction of ifm-3 into lyt-1- and flaA4-containing strains led to partial suppression of the nonmotile phenotype. The possibility that the cellular concentration of autolysins is regulated by the expression of fla genes is discussed. Discrepancies with respect to previous mapping of flaA and flaB are accounted for.