Abstract
Salmonella phage ε15 goes under host-controlled variation (Uetake and Nakagawa, 1960; Toyama and Uetake, 1961; Uetake et al., 1962). ε15 propagated on Salmonella anatum (=A) shows EOP (efficiency of plating) of about 10-2 on cells of Salmonella butantum (=I-1), while ε15 propagated on cells I-1 shows EOP of 10-4 on cells A.
However, when growing cells of I-1 are heated at 49°C for 2-3 minutes, transferred back to 37°C, and infected with phage ε15[A], the proportion of plaque formers to infected cells increases up to 4-6×10-1. It indicates that thermolabile factor (s) is responsible for HCV.
When cells of I-1 are heated after infection with ε15[A], the heat effect on EOP decreases with increasing time elapse prior to heating, indicating the irreversible inactivation of injected phage DNA.
When cells I-1 are heated at 49°C for 3 minutes, transferred back to 37°C, and thereafter aliquots are infected with ε15[A] at time intervals, elavated EOP falls down back to original 10-2 in about 30 minutes, suggesting de nove synthesis of the responsible factor (s). This recovery from the heat effect is completely suppressed by blocking protein synthesis with chloramphenicol, while not affected by clocking DNA synthesis with mitomycin C.
These findings altogether indicate that some thermolabile factor (s) of protein nature is responsible for HCV, which may possibly inactivate injected DNA of restricted phage.
