94 M. R. Pollock 



can be clearly shown to differ qualitatively in the same and 

 closely related organisms (e.g. the human haemoglobins, 

 cattle p-lactoglobulins, etc.) it is often too readily assumed 

 that the respective synthesizing systems have arisen from one 

 another by a single mutation. So far there is no direct evidence 

 to show that this is so. 



Again, in cases where some enzymic activity appears to 

 be lost (or gained) on mutation, it is becoming increasingly 

 apparent that the loss or gain is not absolute and that the 

 "loss" strain (whether mutant or wild type) is suffering from 

 a block that (to use Bonner's terminology) is "leaky". Even 

 in cases where none of the relevant biochemical activity can 

 be detected [e.g. the apparent lack of glutamic acid dehydro- 

 genase in an a-amino acid-requiring mutant of Neurospora 

 (Fincham, 1954)] some hesitation is justified before conclud- 

 ing that the loss is absolute. Quite apart from the possibility 

 that the assay technique is insufficiently sensitive, even a 

 demonstration that there is less than one molecule per cell 

 of a certain enzyme, has no special significance (in relation to 

 this particular point) in organisms which reproduce by binary 

 fission — as long as the synthesizing system is genetically 

 stable. 



Now, there can hardly be any doubt that during the course 

 of evolution qualitative changes in enzymes do occur. Unless 

 there is some quite inconceivable degree of convergent 

 evolution, the systems synthesizing human haemoglobins A, 

 S, C, D and E, for instance, must have evolved either from 

 each other or some common ancestor. The question is there- 

 fore not whether qualitative heritable changes in protein 

 occur; but how frequently and by what means do they occur? 



So far, the proved results of single mutations as expressed 

 in terms of proteins seem to be purely quantitative. Is it 

 therefore not possible that qualitative changes (at the protein 

 molecular level) never in fact result from single mutations as 

 studied in the laboratory? To use Beadle's terminology: can 

 single mutations ever be (at a molecular level) neo-morphic? — 

 or are they always hypo- or hypermorphic? Or do single 



