360 BACTERIOPHAGES 



phage per unit of bacterial surface ratlier than per bacterial 

 cell was assumed, the calculated survival curves fitted Dulbecco\s 

 experimental values well enough to v^alidate the original hy- 

 pothesis. Thus Cairns and Watson attributed the discrepancies 

 to a faulty assumption rather than to a faulty theory. With 

 very heavy doses of radiation, only a small fraction of the mul- 

 tiply-infected bacteria would show multiplicity reactivation and 

 these would be the cells that had adsorbed the largest number 

 of phage particles. With a skewed distribution of cell size, the 

 largest cells would have adsorbed the most phage particles and 

 the proportion of heavily infected cells in the population would 

 be underestimated by the Poisson distribution. 



This explanation of Dulbecco's results was disputed by Harm 

 (1956) on experimental grounds. If the discrepancy between 

 observation and theory is due to the high multiplicity of infection 

 of filamentous cells, it should be possible to decrease the discrep- 

 ancy by removal of the filaments. Filtration of a washed, con- 

 centrated bacterial suspension through fritted glass filters re- 

 moved essentially all filamentous forms, leaving a much more 

 homogeneous cell suspension. The dose-survival curves were 

 the same whether the filamentous cells had been removed or 

 not. This result is difficult to explain unless the filamentous 

 cells have no greater efficiency of multiplicity reactivation than 

 normal cells regardless of how many additional phage particles 

 they have adsorbed. Harm suggested that his data as well as 

 those of Dulbecco might be explained by assuming that in a 

 part of the DNA damages are reactivated by recombination 

 with a probability of essentially one, whereas the efficiency of 

 multiplicity reactivation is fairly low in another part of the DNA. 

 The theory of two different kinds of lethal damage was first 

 proposed by Barricelli (1956). One kind of damage involves 

 ordinary gene loci. The probability of inactivating any given 

 gene locus is very small in comparison with the probability of 

 inactivating the phage particle. This kind of damage can be 

 corrected by genetic recombination in multiply-infected cells 

 providing the damaged regions are not overlapping. The 



