II ORGANOGENESIS 733 



Antimyogen, on the other hand, generally stimulated growth and development. 

 Antiactin and antiglobulin did not seriously affect the embryos. 



We cannot resolve the dilemma created by the results of Ebert, Rose and Weiss. 

 Since all three sets of data are exploratory, seeking to explain cellular events at a 

 molecular level, it is too soon to expect a complete solution of the problem. It is 

 apparent that Ebert's data indicate a selective up-take of homologous tissue 

 proteins or protein constituents and that these have the effect of promoting growth 

 selectively, presumably through increasing the mitotic rate. Rose's data seem 

 to indicate a prevention of differentiation of embryonic tissues by homologous 

 adult tissue extract. Though Rose suggests a theoretical mechanism to account 

 for his results we cannot be certain that this mechanism operates, but almost 

 certainly the mechanism suggested would not apply to the data of Ebert which 

 are apparently concerned with the process of mitosis. Weiss, using a method 

 different from that of either Ebert or Rose, adds still a different variable, namely, 

 organization. His data appear to suggest that in tissue culture, absence of extract 

 of homologous tissue favors differentiation; but his criteria for differentiation can 

 hardly be equated: in the heart tissue, presumably we are concerned with the 

 formation of contractile proteins, and in the kidney we are concerned with the 

 orientation of cells with respect to each other (in addition to increase in mitotic 

 rate, which almost certainly has a different explanation). Ebert, Rose and Weiss, 

 then, have used different experimental materials and different methods; their 

 data have application to different problems. Each of the contributions has merit 

 which will be more fully appreciated when auxiliary and supplementary details 

 of each system have been supplied. 



£. Genetic control of growth. Because of its obvious relation to economics a wealth 

 of data exists on genetic control of growth rate and final attained size in a variety 

 of poultry and mammals. These are painstakingly and thoughtfully reviewed by 

 Dickerson (1954). The data point to the fact that "growth is influenced by 

 inherited differences both in the individual's own growth impulse and the direct 

 nutritional influence of the mother, as well as by uncontrolled environmental 

 factors". In short, Dickerson reiterates the conclusion of genetic relationship to 

 growth, but in the face of the data is quite helpless to specify gene-related me- 

 chanisms. It is only a first approximation to assign from the collected data a role 

 in "control of growth rate through effects on specific nutrient requirement, on 

 endocrine activity, and on sensitivity of response to hormones". One is inclined 

 to be impressed by the observation of Landauer (1952b): "It is important that 

 we should not deceive ourselves. Our knowledge concerning the hereditary forces 

 governing normal embryonic development, of the chick or any other vertebrate, 

 is practically nil." 



This view is probably unduly cynical. Development is the integration of 

 processes of growth, differentiation and maintenance. The metabolic pathways 

 in synthesis are at least partially known in view of data supplied above. What is 

 actually sought, therefore, is confirmation of a genetic mechanism related to 

 significant metabolic processes. There is no lack of such data. The preceding 

 review has shown adequately that the three animals most often vised for embryo- 



Lilerature p. 744 



