Role of Preformed Structure in Cell Heredity 209 



losses over a number of fissions were earlier reported by Faure- 

 Fremiet (1948a) for Leucophrys patula: asymmetric reduction in the 

 number of kineties led inevitably to loss of one set of cortical struc- 

 tures from doublets. Likewise, Hanson ( 1962 ) has noted progressive 

 changes. Localized irradiation of one oral apparatus of a doublet with 

 a fine beam of ultraviolet inflicts damage on the exposed oral appara- 

 tus and on the capacity to produce new ones on that meridian at 

 fission. Both of these kinds of damage, without further irradiation, 

 can independently lead to greater or lesser abnormality over the 

 course of a considerable number of fissions until one or the other of 

 two stable conditions is reached: complete loss of one oral apparatus 

 and the capacity to produce one on that oral meridian, or complete 

 normality. 



Observations like these are important in at least two respects. First, 

 they show that morphogenesis and cell heredity of particular cortical 

 structures are not all-or-none phenomena. The initiation of a cortical 

 structure is only the first step in its creation. Initiation alone does 

 not assure complete normal development. For the latter, other factors 

 are involved. Apparently, there is a sequence of such factors, the 

 operation or effect of later factors in the sequence being dependent 

 upon the normal or abnormal results of the operation of earlier factors 

 in the sequence. The nature of these factors and of their operation in 

 ciliates is almost totally unknown, although initial attempts to under- 

 stand them have been made by Faure-Fremiet (1948a) and Hanson 

 ( 1962 ) . 



Second, observations of these sorts, by providing an example of 

 progressive cortical changes over a series of successive fissions, may 

 provide a connection in principle between the short-term phenomena 

 of cell heredity and morphogenesis and the long-term progressive 

 changes in morphogenesis and cell heredity, extending over hundreds 

 of successive fissions, that constitute the clonal life cycle of imma- 

 turity, maturity, senescence, and death (Maupas, 1888; Calkins, 1926a; 

 Sonneborn, 1954c; Jennings, 1944). Among the events of clonal aging 

 is an increasing frequency of abnormalities of cortical structures and 

 of abnormalities in the processes of production of cortical structures 

 at fission (Sonneborn and Schneller, 1955; Sonneborn and Dippell, 

 1960b ) , including final failure to form at fission an oral apparatus 

 (Dippell, 1955). The basic mechanisms underlying this one-way 

 progression away from "normality" (i.e., the condition in young 

 clones) may be similar to those operating in the progression toward 

 complete loss of one set of oral organelles from doublets. Further 

 analysis of either may throw light on both. 



