Genetics of motility in Escherichia coli: complementation of paralysed mutants.

LTHOUGH flagella are regarded as the bacterial motor organs and have been A extensively studied, little is still known about the mechanism of their action (for a review see WEIBULL 1960). One approach to an understanding of the movement of flagella has been the study of mutants defective in motility. Nonmotile flagellated strains of Salmonella have been known for many years (COLQUHOUN and KIRKPATRICK 1932; KAUFMANN 1939; EDWARDS, MORAN and BRUNER 1946; HIRSCH 1947; FRIEWER and LEIFSON 1952). Such variants have generally been referred to as “paralyzed” and those examined in detail were found to have flagella in typical number and shape and to agglutinate with antiserum prepared against wild-type flagella. Most Salmonella can alternate between making one or the other of two kinds of flagella (phase variation), each a polymer of an antigenically different flagellin (MCDONOUGH 1965). The two flagellins are determined by different genes, designated HI and H2, yet paralyzed strains are nonmotile no matter which flagellin is being made. This observation suggests that the mutation affects some factor responsible for the functioning of the flagellum other than flagellin. Genetic studies on Salmonella have confirmed this conclusion (MITANI and IINO 1965), and the results reported in this paper show that the same is true of Escherichia coli. In addition, we have investigated the number of paralyzed complementation groups and their relationship on the bacterial chromosome. Complementation tests have already led to the classification of paralyzed mutants of Salmonella typhimurium into three groups ( ENOMOTO 1962,1966). General description of the complementation test: In a transduction, the bacteriophage carry small fragments of the donor chromosome to the recipient bacteria. In complete transduction, donor genes transferred by the phage replace their alleles on the recipient genome. STOCKER, ZINDER and LEDERBERG (1953), studying the transduction of flagellar characters by the Salmonella phage P22, observed not only swarms, arising from the complete transduction of motility to nonmotile strains, but also trails: linear groups of microcolonies extending out from the site of inoculation (see, for example, Figure 1 ) . A trail marks the path of a bacterium made motile by abortive transduction (STOCKER 1956; LEDERBERG 1956). In such an abortive transduction, the wild-type motility gene introduced by the phage neither recombines with the recipient genome, nor multiplies. It is, ’ Suppot trd by giants from the (1 5 Public Health Service and the YTational Reseach Council, Canada

[1]  B. Stocker,et al.  Complementation of non-flagellate Salmonella mutants. , 1965, Journal of general microbiology.

[2]  M. Mandel,et al.  Optimal conditions for mutagenesis by N-methyl-N′-nitro-N-nitrosoguanidine in escherichia coli K12☆ , 1965 .

[3]  J. Lederberg Linear Inheritance in Transductional Clones. , 1956, Genetics.

[4]  A. B. Moran,et al.  Flagella and Flagellar Antigens in “Non-Motile” Salmonella Cultures.∗ , 1946, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.