CONTROL BY REPRESSION 57 



Magasanik et al. (1958) pointed out that lepressihilitv l)v glucose 

 seems to be characteristic of enzymes whose physiological role is to 

 supply energy, carbon, or nitrogen by the degradation of organic 

 compounds (e.g., yS-galactosidase, "galactozymase," inositol dehy- 

 drogenase, glycerol dehydrogenase, histidase, tryptoplianase, and 

 amino acid deaminases). Repression of the formation of such "en- 

 ergy-supplying" enzymes by products of glucose metabolism would 

 be comparable to the repression of an enzyme in, say, a path of 

 amino acid s\'nthesis by the "end product" of the patli. 



Recently, Neidhardt ( 1960b ) has discussed the mechanism of 

 the glucose effect and has reyiewed ayailable eyidence in the light 

 of the notion that this effect represents enzyme repression. Cohn 

 and Horibata (1959b) haye presented an extensiye analysis of the 

 mechanism of glucose antagonism to yS-galactosidase formation; their 

 results are consistent with an interpretation of this case of the glu- 

 cose effect in terms of enzyme repression. 



Comments on the General Biological Significance of Repression. 



It seems clear that control by repression applies to a wide yariety 

 of enzymes in a diyersity of metabolic systems. In general, repres- 

 sion has been studied in linear or cyclic pathways capable of sup- 

 porting a substantial flow of metabolites through them. It may, 

 howeyer, well be that certain kinds of enzymes are not subject to 

 such control. This possibility is suggested, for example, by the 

 finding of Ames (1960) that the histidine-actiyating enzyme of S. 

 tijpJiimuriiim, in contrast to the enzymes of histidine synthesis, is 

 not repressible by this amino acid. Pardee (1960) has discussed 

 the question of the control of systems, such as those of coenzyme 

 synthesis, for example, that carry a relatiyely small flow of metab- 

 olites. 



For the regulation of cellular function, the frequently obseryed 

 cooperatiye action of repression and feedback inhibition seems par- 

 ticularly significant. Control by feedback inhibition is rapid; pre- 

 sumably, it makes itself felt as soon as a sufficient concentration of 

 the inhibitor is built up in the yicinity of the susceptible enzyme. 

 Repression, as a mechanism capable of controlling the flow of me- 

 tabolites through a pathway, acts relatiyely slowly, despite the 

 promptness with which the onset of repression can occur: repression 

 decreases the rate of enzyme formation; it does not interfere with 

 existing enzyme molecules (whose concentration in the cell can 



