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Arthur L. Koch 



account for the mutational activity of these methylated purines. So far we have 

 been unable to detect any such differences. We may have been examining the 

 wrong systems. 



For the present we shall tentatively suggest the pair thymine-cytosine (Fig. 5) 

 as the culprit. This pair is shorter than the conventional structures. In the 

 very interesting paper by Donohue (16) a large number of possible pairings 

 are suggested. For our purposes most of these are unsatisfactory because they 

 give rise to helices possessing a two-fold axis parallel to the hehcal axis, whereas 



thymine cytosine 



Fig. 5. 



in the Watson-Crick structure this two-fold axis is perpendicular to the 

 helical axis, and thus consistent hehces formed by substitution between the 

 two types can not occur. One structure (Donohue's no. 22) would fit into the 

 symmetry of the Watson-Crick model and it is the pairing suggested in Fig. 5. 



VI. STEADY-STATE CONSIDERATIONS 



Whatever may be the critical or quantitatively most significant substitution 

 in this type of mutational change, the hypothesis we have proposed requires 

 that the concentration of terminal pools be altered. The experimental data 

 that we have obtained have been primarily with purine ribonucleoside phos- 

 phorylase which catalyzes a step which is clearly non-terminal in DNA synthesis, 

 and very likely the reaction catalyzed by purine deoxyriboside phosphorylase 

 is also not the transformation of the last small-molecular-weight intermediate 

 into DNA. 



Although it may be that the terminal processes are inhibited, let us examine 

 some possible situations that might lead to an alteration of the steady-state 

 concentration of the penultimate substance without influencing the steady-state 

 flux of DNA synthesis. To do this, the question of bacterial growth itself must 

 be raised. Bacteria grow autocatalytically. Hinshelwood (17) as well as 

 others have pointed out that this results from an interaction of catalytic units. 

 Thus, if the amount of one component, P (protein), controls the rate of synthesis 

 of another component, N (nucleic acid), then 



dP 



dt 



dN 

 ~di 



k,P 



(1) 



