148 THE BIOSYNTHESIS OF PROTEINS 



1948; Spiegelman et al, 1951; Campbell and Spiegelman, 1956). A clear 

 distinction is made here between autoduplicating particles like genes or 

 viruses, which carry structural information for their own multiplication, 

 and aiitocatalytic objects which are required, albeit remotely, for the 

 formation of identical objects because they fulfil a certain biochemical or 

 biophysical function. In this broad sense, all the 'indispensable' enzymes 

 of a living cell are autocatalytic objects, and so are many other cell con- 

 stituents, e.g. the phospholipids of the membranes. For if the activity of 

 the enzyme is blocked or if the phospholipid is destroyed, the cell dies and 

 stops making the enzyme and the phospholipid. 



If the physiological activity of an autocatalytic object X was required for 

 the synthesis of the respiratory enzymes, but completely unnecessary for 

 the life of the cell and for its multiplication, that autocatalytic object would 

 indeed have many properties in common with the 'extrachromosomal 

 hereditary factor' of yeast. Accidental loss or destruction would obviously 

 deprive the cell of the capacity of making the respiratory enzymes and of 

 perpetuating the factor. 



But it must be clearly realized that the loss of the object X per se is not 

 the essential thing; what is all important is the disappearance of the 

 biochemical or h'lo-ph.y&icdX function that it normally fulfilled. This special 

 feature of the autocatalytic particle has two fundamental consequences. 

 The first is that any inhibitor of the activity or function of X is a potential 

 mutagen. If the biochemical activity or the biophysical futiction of the 

 object X is interrupted, the synthesis of more X is blocked, together with 

 that of the respiratory enzymes. In resting cells, the only observable fact 

 will be the inhibition of the synthesis of the respiratory chain. But if the 

 cells do multiply, while X cannot, X will be lost by dilution for part of 

 the progeny, and mutants will appear. This is exactly what happens in the 

 presence of euflavine in yeast. Euflavine first inhibits the synthesis of the 

 respiratory enzymes, and respiratory mutants appear a few hours later 

 (Slonimski, 1953; Marcovich, 1958). Among the acridines, only those 

 which specifically interfere with the synthesis of cytochrome oxidase are 

 mutagenic (Slonimski, 1953). A fairly good correlation between the condi- 

 tions which depress chlorophyll synthesis and those which favour mutation 

 in Eiiglena was also observed by De Deken-Grenson (1960) who suggested 

 that the hereditary transformation might be a consequence of the primary 

 phenotypic inhibition of chlorophyll synthesis. 



A second consequence of the properties of an autocatalytic object like X 

 is that its loss is not irreversible-by-nature as would be that of a structural 

 gene. It will be reversible or irreversible depending on whether or not the 

 function normally accomplished by X can be temporarily fulfilled by an 

 action of the experimentator, or due to a change in conditions. This will 

 indeed restore the synthesis of X which will then take over its normal 



