Section 3 — Molecular and Microbial Genetics 



of its DNA, has been of vivid interest to both 

 biochemists and geneticists. We therefore 

 studied some properties of host-phage rela- 

 tionships with this phage. 



Plating wild type E. coli CI 22 with an excess 

 of wild type OX- 174 will result in the selection of 

 phage-resistant bacteria (designated by C/0). 

 Among them three types of C/0 mutants could 

 be distinguished, on the strength of differences 

 in the frequence with which plaques of host- 

 range phage mutants (Oh) were found after 

 plating C/O cells with wild-type phage. 



The largest class, some 80 per cent of all 

 C/0 isolates, comprises the mutants for which 

 no host-range particles (i.e. less than 10 _u ) 

 were observed in wild-type lysates, not even 

 after heavy mutagenic treatment with nitrous 

 acid. These bacterial strains (C/OR) are consid- 

 ered to be resistant to all first step host-range 

 mutants. On a second type of C/O bacteria 

 ("normal", C/ON) small, turbid host-range 

 mutant plaques (Oh n ) were found with a fre- 

 quency of 3 x 10~ 9 . From Oh n , but not directly 

 from wild-type phage, mutants yielding clear 

 plaques could be isolated (0h c ). The host- 

 range patterns of independently isolated strains 

 of 0h n and Oh c are identical for all C/O in- 

 dicator strains. A third, extremely rare, type of 

 C/O mutants ("sensitive", C/OS) was charac- 

 terized by a higher frequency (4 x 10~ T ) of large, 

 clear plaques of host-range mutants (Oh s ) 

 found after plating with wild-type phage. C/0S 

 also served as a host for 0h n and Oh c . On the 

 other hand, C/ON was resistant to Oh s . 



Results obtained, using Shigella paradysen- 

 teriae Y6R as the host bacterium, partly paral- 

 leled those with E. coli. 



Our findings will be discussed in relation to the 

 mechanism of phenotypic expression of bacte- 

 rial resistance and host-range properties of the 

 phage. 



3.20. Studies of Proteinless Mutants of Tobacco 

 Mosaic Virus. A. Siegel and M. Zaitlin (Tuc- 

 son, U.S.A.). 



Two mutants of tobacco mosaic virus have 

 been isolated which are unable to induce the 

 formation of complete virus particles upon in- 

 fection. Strain PM 1 induces the formation of no 

 detectable virus-like protein. Strain PM2 induces 

 the formation of a non-functional, low molecular 

 weight protein serologically related to tobacco 

 mosaic virus protein. This virus-like protein, 

 although it aggregates into rods under slightly 

 acidic conditions, will not reconstitute with 

 virus nucleic acid to form complete virus parti- 



cles. The PM2 protein differs from parent strain 

 protein in one of the first forty amino acids, 

 starting from the acetyl-N end. Infectious ma- 

 terial present in phenol extracts of PM infected 

 leaves can be reconstituted with virus protein to 

 form highly infectious particles. It has also been 

 found that infectious nucleic acid can be sep- 

 arated from the bulk of the leaf RNA on 

 methylated albumin columns. 



3.21. Hereditary Changes induced by the Host in 

 Bacteriophage Lambda. L. Fischer-Fantuzzi 

 and E. Calef (Naples, Italy). 



A particular strain of K12 sensitive to lambda 

 (called U 173) upon infection with the hdi 

 mutant of bacteriophage lambda yields wild 

 type progeny phage or lysogenic derivatives 

 which in turn will release wild type phage. 



Both vegetative and induced phage appear to 

 be mixed, wild type and mutant. 



The wild type and the mutant obtained from 

 the growth on strain U 173 breed true. 



This hereditary modification is associated with 

 the appearance of phages of non standard 

 density. 



3.22. The Genetic Nature of the Exclusion of Bacte- 

 riophage T2 by T4 with Mixed Infection on 

 E. coli B. B. de Groot (Leyden, The Nether- 

 lands). 



Cross products of bacteriophage T4 and T2 

 show the efficiency of plating (e.o.p.) of T4 on 

 certain E. coli K strains; they have the same 

 glucose-substitution of HMC as T4, and the 

 frequency of T4 markers is about 90 per cent. 

 This phenomenon, the exclusion of T2 by T4* 

 has been ascribed to one gene ("Bar") by Strei- 

 singer and Weigle.^ 1 ) The genetic nature of 

 exclusion was investigated in the following ways: 



(1) Single bursts of T4 T2 crosses were ana- 

 lyzed completely. The majority of the progeny 

 particles showed the T4 host range. A few of 

 them showed either the u.v. sensitivity of T2, 

 or did not exclude the markers of T2, or appear- 

 ed to plate with a low e.o.p. on E. coli K strains, 

 like T2. 



(2) Simultaneous infection of E. coli B with 

 heavily u.v. -irradiated T4 and unirradiated T2 

 resulted in marker rescue of the e.o.p. of T4, 

 when plating the infective centres on E. coli 

 K (A h). An isolated marker-rescue product did 

 not exclude T2 markers on crossing. Both these 

 experiments suggest that the "Bar"-properties. 



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