52 CONTROL MECHANISMS IN CELLULAR PROCESSES 



some metabolism and propagation, as discussed in The Site Prob- 

 lem. It may thus well be that (functional) repressors impede the 

 separation of nascent enzymes from their templates and, thereby or 

 independently, interfere with ribosome propagation. Inducers (in 

 functional form) would have an opposite effect through antagoniz- 

 ing a repressor or conceivably through "positive" induction. 



The notion of a dual effect of repressors on enzyme formation and 

 on ribosome propagation has received a measure of support from 

 the pace-setting phenomenon described in an earlier section and 

 discussed below. 



Pace-setting Effect and Site of Repression. Upon variation 

 of the point of onset of acetylornithinase derepression, it was found 

 that the later the onset, i.e., the longer the period of prior repression, 

 the lower is the subsequent differential rate of derepressed enzyme 

 formation ( Fig. 2-2 ) . Although several interpretations of this pace- 

 setting effect are possible, the most adequate working hypothesis 

 would seem to be that, in addition to repression of acetvlornithinase 

 formation by arginine, there is a repression-like antagonism, appar- 

 ently also by arginine, to the formation of a component, or com- 

 ponents, of the corresponding enzyme-forming system. It is assumed 

 that the differential rates of acetylornithinase formation reflect the 

 number of corresponding functional enzyme-forming sites available, 

 per unit mass of the organisms, at the point of onset of derepression. 

 During the period preceding the onset of derepression, while acet- 

 ylornithinase is being repressed, the number of such sites per unit 

 mass of organisms would decrease, and on subsequent derepression 

 the pace-setting effect would become apparent. 



The proposed dual effect, at the secondary-template level, on (a) 

 the production of the enzyme molecules and (b) the production of 

 the enzyme-forming sites can be readily visualized in terms of the 

 possible metabolism and propagation-type behavior of ribosomes 

 (see the discussion The Site Problem). Conceivably, the very act 

 of binding, contemplated in the regulator hypothesis, of the nascent 

 enzyme molecule to its template may interfere with the postulated 

 splitting-and-reutilization behavior of the ribosomes; alternatively, 

 the repression of enzyme formation and the interference with ribo- 

 some propagation may be somewhat less directly related. Accord- 

 ing to this general model, the repressor site (i.e., the region of the 

 ribosome-nascent enzyme complex for which the functional repressor 



