REGULATION 149 



function. A beautiful illustration of such a phenomenon is the loss and 

 recovery of galactosidase synthesis in E. coli. The factor X here is obviously 

 the permease. It is an autocatalytic object, since its function is to pump 

 galactosides into the bacterium, and since the achievement of a certain 

 concentration of galactoside within the cell is required for the induction of 

 permease formation and /S-galactosidase synthesis. Loss of the permease 

 occurs during growth under conditions which abolish the function of the 

 permease, e.g. when there is no galactoside available to be pumped into the 

 cell. Loss of the permease is reversible because when a sufficient concentra- 

 tion of galactoside is applied from the outside, free diffusion can com- 

 pensate momentarily for the function of the permease, and thus induce its 

 formation, together with j3-galactosidase synthesis. The adapted state can 

 then be transmitted clonally as long as the conditions allow the permease to 

 function. Long-term adaptation of yeast to galactose, for which the model 

 of autocatalytic particle was first proposed (Campbell, 1960) is another 

 example of reversible loss of the particle. 



In other cases, of course, the loss will be irreversible for all practical 

 purpose simply because it will be impossible to compensate for the bio- 

 chemical or biophysical function of the autocatalytic factor long enough to 

 allow the synthesis of it to be restored. For instance, if the function of the 

 autocatalytic factor is to be an essential piece of some subcellular structure 

 it might be altogether impossible to restore this function from the outside. 



The concept of an autocatalytic object which does not carry any genetic 

 information but simply accomplishes a certain physiological function 

 necessary for its own formation and eventually for other anabolic processes 

 as well, thus leads to a general theory which accommodates cytoplasmic 

 heredity and other phenomena which mimic heredity. Besides, it leads to 

 predict puzzling and somewhat conflicting features of cytoplasmic 

 heredity: the loss of the cytoplasmic factor as if it occurred by dilution of 

 particles, the mutagenic effect of inhibitors of certain enzyme synthesis. 

 The unstable state in which yeast or Eiiglenae can exist after a threshold 

 treatment by the mutagen might be a state in which the activity of X is just 

 sufficient to insure its own synthesis but not that of the enzymes; slight 

 changes of the medium can tilt the equilibrium either towards recovery or 

 towards irreversible loss. 



Any theory can of course be stretched to accommodate any experimental 

 facts and it would be without interest for the present discussion to elaborate 

 further the concept of autocatalytic element. This model is presented in an 

 attempt at making a unifying synthesis. The only merit that it claims is of 

 placing old facts in a new perspective and, in so doing, of suggesting new 

 experiments. 



Whatever the ultimate nature of the non-mendelian factors in enzyme 

 synthesis may be, it is becoming more and more probable that these factors 



