Role of Preformed Structure in Cell Heredity 215 



analysis, proved that the difference between two hereditary cortical 

 types, singlets and doublets, was not due to any genie, nuclear, or 

 endoplasmic difference. Finally, natural grafts of a piece of cortex 

 showed that it was decisive in morphogenesis and cell heredity. The 

 autonomy and genetic significance of cortical structure was thus fully 

 established. 



We then tried to pin down just what cortical structure is genetically 

 autonomous and just how this genetic autonomy is achieved. Con- 

 spicuous cortical structures, like kinetosomes, kineties, and groups of 

 kineties, to which a causal role in morphogenesis and cell heredity 

 has often been attributed ( and still is, in many quarters ) , are clearly 

 not genetically fixed as to their developmental and genetic roles. They 

 are one instrument, not the cause, of morphogenesis and cell hered- 

 ity. They are responsive to, and express visibly, the more basic, under- 

 lying causal cortical structure. This finer structure, probably at the 

 molecular level, is the basis of the genetically and morphogenetically 

 decisive interactions we have described as occurring between juxta- 

 posed diverse cortical areas which are the seats of gradients of struc- 

 ture and action. 



What are the determinative molecular species, configurations, and 

 modalities in the cortex? At present this remains almost or quite 

 completely unknown, not only in ciliates but in all organisms. Faure- 

 Fremiet ( 1950, 1954 ) has put forth stimulating suggestions based 

 upon the general geometrical parallels between kineties and macro- 

 molecules such as polypeptides and polysaccharides. He points out 

 that both exhibit similar symmetry, polarity, and other polymeric 

 features. He suggests tha* the properties of the visible structures are 

 consequences of the comparable properties of the constituent and/or 

 surrounding cortical macromolecules. This suggestion is attractive, 

 but alone it of course does not account even in principle for the 

 modalities of morphogenetic processes and their genetic consequences. 



How can we in general bridge the gap between the (unknown) 

 molecular structure of the cortex and the morphogenetic and genetic 

 processes which surely are linked to it? Speculation about the answer 

 to this question cannot be entirely free; it must be limited to conform 

 with a good deal of pertinent knowledge. In particular, it must con- 

 form with what is known about nuclear functions. The cistrons or 

 genes make polypeptides, proteins, enzymes, and indirectly the prod- 

 ucts of enzymic activities. Some of these doubtless enter into the com- 

 position of the cortex of the cell. Differences between allelic cistrons 

 or genes would therefore be expected to result in molecular differences 

 in the cortex and thus to determine at least some cortical differences. 



