Abstract
The idea that the two phenomena, host-range mutation and host-controlled variation may be merely superficially different from each other, but principally two sides of a single matter, arose to us at first when we were studying “semi-resistance” of the bacterium to the bacteriophage (Nojima and Fukumi, 1954b) . It was further developed when the so-called host-range mutations of T3 bacteriophage were investigated from this point of view (Fukumi and Nojima, 1954) . The fundamental difference of our thought from the current view of host-range mutation lies in the following point; namely, if the bacteriophage a possesses the inf ective titers of 109/cc on the host microorganism A and of 103/cc on the resistant host A/a, one usually understands according to the current view that 103 particles of the host-range mutant of phage a being capable of attacking the resistant host A/a exists among 109 particles of the original phage a, while according to our view, it is explained so that the phage a possesses 10-6 of efficiency of plating (EOP) on the resistant host A/a in comparison with its value 1 of EOP on the original host A.
The fact that a number of phenomena concerning host-range mutation of T3 phage can be explained only partially by the current theory has already reported by Fraser and Dulbecco (1953) and Hershey, Garen, Fraser and Hudis (1954) besides us. However, no reasonable explanation has been presented so far by any of the workers.
The presentation alone of the facts that are impossible to explain is not of constructive nature, and as even the consideration described by us in the previous paper (Fukumi and Nojima, 1954) does not include, fundamentally speaking, any understandable analysis from genetical point of view, it may have at most confused or irritated some workers.
In the present paper, we are going to present aa theory capable of explaining genetically the difficulties mentioned above. The theory has been constructed by us from the suggestions of Hershey, Garen, Fraser and Hudis (1954), and of Demerec (1956) . The former workers have suggested that the host-range mutants of T3 bacteriophage arise by interactions between phage and bacterium, possibly in the nature of genetic substitutions, while the latter have explained the transduction by the cross-over between the host genes and the phage genes.
Before the theory is presented, some data concerned with the host-range mutations of T1 phage, which are also impossible to explain by the current view will be described at first.
