The interaction of 12 phage strains with bacilli, protoplasts, and L forms of Bacillus subtilis 168 and with eight of its mutants and two of its lysogens is described qualitatively and quantitatively. After removal of the cell wall from B. subtilis 168, 11 of the 12 phage strains can still adsorb to the protoplasts, nine kill their wall-less host cells, and five multiply in the naked bacteria, forming plaques on L form lawns. Individual gene mutations can have similarly pleiotropic effects, strongly dependent upon the plating medium. Thus, the gta A mutation, which causes loss of glucosylation of the wall teichoic acid, results in loss of wall adsorption sites for 029 (but not membrane sites) and for X105. Phages X25, SP82G and oe can still adsorb to gta A bacilli and plaque in unstabilized and sorbitol-stabilized lawns of this mutant, but they can not plaque in sucrosestabilized lawns. The lysogenized wild type, B. subtilis 168 (SP02), also exhibits a pleiotropic pattern, showing different levels of resistance to phages SP02, X1, 4e, and 025. Its resistance pattern is very similar to that of wild-type protoplasts. On the basis of such patterns, the bacterial mutants and strain B. subtilis 168 strain 4)1

Adsorption of bacteriophages 429 and 22a to protoplasts of Bacillus subtilis 168 is described. The number of binding sites on bacilli and protoplasts is determined for each phage. Bacilli and protoplasts possess roughly the same number of sites per unit area for 429, i.e., approximately 700 sites per bacillus.