244 ERNST FREESE 



UV hit^ to inactivate the rll function (Kric^, lOoOa) or an rll marker 

 (Docrniann ct (iL, 19')o) than to inactixatc the phage. For a review see 

 Stalil (1959). 



Attempts to induce mutations l)y the UV-irradiation of free phages 

 have often been unsuccessful (Weigle, 1953; Latarjet, 1954) while 

 irradiation of the infected bacteria (Latarjet, 1949, 1954; Weigle, 1953; 

 Weigle and Dulbccco, 1953; Tessman, 1956) or even of the bacteria 

 alone before infection (Jacob, 1954; Fraser, 1957 1 leadily produccHl 

 UV-induced phage mutations. In some cases these ''mutations" may have 

 been caused by a radiation-induced recombination process between the 

 phage and the bacterial genome (Stent, 1958) excejit for bacteriophages, 

 like T2 or T4, which do not seem to have any similarity to the host 

 genome (very different base ratio and Hj\IC in their DNA). A very 

 small direct effect has been reported by Tessman (1956) for phage Tl. 

 A significant induction of reverse mutations of a T4 rll mutant by 

 UV-irradiation of free phage has been shown by Krieg (1959b). To 

 prove the effect it was necessaiy to inactivate the phages quite strongly 

 and then to infect the bacteria in high multiplicity; it is not clear 

 whether revertants can be induced by some mistakes in multiplicity 

 reactivation. Another direct effect is reported by Ellmauer and Kaplan 

 (1959) for the phage K of Seiratia marcescens. 



In bacteria the possibility of an indirect induction of mutations by 

 UV has been clearly established. Stone et al. (1947) showed that the 

 UV-irradiation of bacterial media produced mutagens which induced 

 nmtations in unirradiated organisms placed in these media within less 

 than 4 hours. The radiation product is apparently unstable and organic 

 peroxides or radicals have been suggested as the cause of mutations. 

 Wyss et al. (1948) have shown that organic peroxides are mutagenic 

 while HoOo in saline is not. But since UV also acts on the pyrimidine 

 bases and the corresponding nucleotides within the bacterium, it is by no 

 means clear how the major mutagenic effect of UV on bacteria comes 

 about. That most UV-induced mutations somehow involve extrachromo- 

 somal material is shown by the observations (Witkin, 1959) that the 

 frequency of UV-induced mutations is reduced when in the innncdiate 

 post-irradiation period protein synthesis is blocked (by lack of amino 

 acids or by chloramphenicol) or altered (by the incorporation of amino 

 acid analogs) or when the formation of purines is inhibited (by non- 

 mutagenic concentrations of caffein). In contrast the frequency of 

 mutations is increased by the addition of nucleic acid bases. The estab- 

 lishment of UV-induced mutations apparently needs the presence of 

 some unstable DNA precursors and DNA synthesis; the majority of 

 potential UV-induced reverse nmtations are established within one bac- 



