380 CELL HEREDITY 



ot chroiuosonuil markers and prt)l)a!)l\ has an cxtrachromosomal resi- 

 (k'licr. This supposition is supported by the fact that flies infected with 

 \irus may be cured by heat shock, some only temporarily. The virus, 

 sifima (ff), may mutate into several other types. But the most in- 

 teresting condition is an association, rho (p), resembling that in lysogenic 

 bacteria, because infected flies are resistant to CO, until a certain age 

 when they become sensitive. In the interim they are immune to infection 

 and do not yield virus. When the viruses are extracted from aged P flies, 

 they are found to be indistinguishable from n taken from other sources. All 

 this is a strong indication of a provirus state, and the transformation into 

 infectious virus upon senescence has implications for the origin of diseases 

 of age. Instances of transduction and lysogenic conversion have yet to 

 be reported. The fact that many animal and plant viruses have R\A as 

 genetic material rather than DNA raises interesting questions in this 

 regard. 



PHENOCOPIES 



A final category of mechanisms by which somatic cells may vary is that 

 of phenocopies. A phenocopy is a phenotype modification which mimics 

 some mutant condition but is not inherited at sexual reproduction. Ex- 

 posure of Drosophila larvae to high temperatures will cause some to 

 develop mutant wings or lozenge eyes, but not because of a change in 

 genotype. Nonetheless, the change does have a somatic hereditary basis, 

 the cells of the soma reproducing the same modification. A fine study of this 

 kindof hereditary mechanism was made by NoN'ick on the induced synthesis 

 of /3-galactosidase in E. culi. When an inducer is present in saturating 

 concentrations, a hnear relation is found between the appearance of new 

 /3-galactosidase and the synthesis of new protein (Figure 12.12). This 

 suggests that all cells participate uniformly in the synthetic process, a 

 concept confirmed by other lines of experimentation. It is otherwise 

 when the concentration of inducer is low; there is then a lag before 

 enzyme synthesis begins at an exponential rate, eventually reaching that 

 observed with high levels of inducer. The accelerating phase of enzyme 

 formation is ascribable to a heterogeneity in the population; only a frac- 

 tion of the cells become capable of being induced at one time; they trans- 

 mit this ability to their progeny. The other cells cannot do this. As 

 may be recalled from Chapter 11, in order for the inducer to enter the 

 cell, a transport enzyme, or permease, must be formed. Once inside the 

 cell, the inducer causes the formation, not only of (8-galactosidase but 

 also of more permease, leading to the transport of more inducer, and so 



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