180 H. MARCO VICH 



differences in the efficiency of rescuing the same selected markers of 

 the Hfr by mating with two different F~ strains, the slope of the sur- 

 vival curve is of little help, if any, for giving quantitative information 

 on the size of the inactivated target, as has been done in a recent work 

 (Wilson, 1960). 



Since no dominant lethals have been found by means of recombination 

 methods two alternative hypotheses may be considered to explain the 

 exponential dose lethal effect relationship in E. coLi. 



1. The lethal effect is not linked to a nuclear damage. Consequently, 

 the inactivated structure should be unique or, if there ^\'ere many, the 

 alteration of one of them would lead to a dominant lethal sequence of 

 events for which w^e have no model to jjropose. 



2. The lethal effect is linked to some action in the nuclear material, 

 but is not transmissible to the zygote. Such effects are known. For 

 instance, induction of phage production by lysogenic bacteria is a 

 dominant lethal effect. The cells are killed in relation to phage synthesis 

 and according to a one-hit dose-effect relationship (Marcovich, 1956). 

 On the other hand, induced phage is not transmissible to the recombin- 

 ants. But this model cannot apply without modification to non-lysogenic 

 or non-inducible lysogenic bacteria. Yet, a starved lysogenic strain 

 loses its aptitude for induction either by u.v. light (Jacob, 1952) or 

 by X-rays (Marcovich, 1957), and still the survival curves are ex])o- 

 nential. On the other hand, starvation does not modify the shape of 

 non-lysogenic or non-inducible lysogenic strains and does not affect 

 their intrinsic radiosensitivity. A working hypothesis to explain these 

 results is that the lethal event in E. coli and the very early stej) in 

 lysogenic induction, are processes of the same nature, if not identical. 

 Experiments are now being done to test the implications of this assump- 

 tion. 



REFERENCES 



FuERST, C. R., Jacob, F. and Wollman, E. (1956). C.B. Acad. Sci.. Paris. 243, 2102. 



Jacob, F. (1952). Ann. Inst. Pasteur 82, 578. 



Latarjet, R., and Ephrussi, B. (1949). C.R. Acad. Sci., Paris, 228, 1354. 



Marcovich, H. (1956). Ann. Inst. Pasteur, 90, 458. 



Marcovich, H. (1957). These, Faeulte des Sciences, Paris. 



Mortimer, R. K. (1955). Radn Res. 2, 361. 



Puck, T. T. and Marcus, P. T. (1!)56)../. exp. Med. 103, 653. 



Puck, T. T., Morkovix, D., Marcus, P. I., and Cieciura, S. J. (1957). J. exp. Med. 



106, 485. 

 Rogers, W., and von Borstel, R. C. (1957). Radn Res. 7, 484. 

 VON BoRSTKL, li. C, and Rogers, R. W. (1958). Rudt} Res. 8, 248. 

 Wilson, D. E. (1960). Radn Res. 12, 230. 



