Jacobson E D, Landman O E
J Bacteriol. 1975 Oct;124(1):445-8. doi: 10.1128/jb.124.1.445-448.1975.
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 phi (but not membrane sites) and for phi105. Phages phi25, SP82G and phie can still adsorb to gta A bacilli and plaque in unstabilized and sorbitol-stabilized lawns of this mutant, but they can not plaque in sucrose-stabilized lawns. The lysogenized wild type, B. subtilis 168 (SPO2), also exhibits a pleiotropic pattern, showing different levels of resistance to phages SPO2, phi1, phie, and phi25. 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 (SPO2) could be ordered into four classes and the phage strains classified into four to six groups. Together, they form four to six interaction complexes, based partly on adsorption sites and perhaps partly on metabolic blocks in phage development.
定性和定量地描述了12种噬菌体菌株与枯草芽孢杆菌168的杆菌、原生质体和L型菌,以及与它的8个突变体和2个溶原菌之间的相互作用。从枯草芽孢杆菌168去除细胞壁后,12种噬菌体菌株中的11种仍能吸附到原生质体上,9种能杀死其无壁宿主细胞,5种能在裸露细菌中繁殖,在L型菌菌苔上形成噬菌斑。单个基因突变可产生类似的多效性效应,这在很大程度上取决于平板培养基。因此,导致壁磷壁酸糖基化缺失的gta A突变,会导致噬菌体φ(但不是膜位点)和噬菌体φ105的壁吸附位点丧失。噬菌体φ25、SP82G和噬菌体φe仍能吸附到gta A杆菌上,并在该突变体的不稳定和山梨醇稳定的菌苔上形成噬菌斑,但它们不能在蔗糖稳定的菌苔上形成噬菌斑。溶原化的野生型枯草芽孢杆菌168(SPO2)也表现出多效性模式,对噬菌体SPO2、φ1、噬菌体φe和噬菌体φ25表现出不同程度的抗性。其抗性模式与野生型原生质体非常相似。基于这些模式,细菌突变体和枯草芽孢杆菌168(SPO2)菌株可分为四类,噬菌体菌株可分为四至六组。它们共同形成四至六个相互作用复合体,部分基于吸附位点,可能部分基于噬菌体发育中的代谢阻断。