GENIC INTERACTION 191 



embryonic development in the strain 129/J, and he found a second critical phase during 

 the eleventh or twelth day of inducing Polydactyly. Is that the second critical stage 

 for genie interaction ? 



Dr. Wright: These critical stages probably have very little to do with the gene 

 under study. There are certain weaknesses in the developmental process leading to 

 the development of Polydactyly, microphthalmia, or anencephaly according to the 

 time of development. Anything environmental or genetic which produces a sufficient 

 disturbance at that critical time would bring out that particular type of defect. The 

 specificity is not so much in the gene, although the timing of genie action may be re- 

 garded as specific ; the character of the effect depends on the developmental background. 

 Also the same gene may bring out other different developmental effects if it comes into 

 play at different times. 



Dr. Steinberg : I hope that in working with mice, investigators will not go through 

 the same series of mistakes that happened when flies were used to detect the time of 

 genie action. When it was found that there is a specific period during development 

 when temperature would affect the size of the eye, it was labelled the temperature- 

 effective period, and it was concluded that this was the time when the gene was acting. 

 However, when the embryology was pursued, it was found that a detectable effect of 

 the gene on the development of the eye occurred some 24 to 36 hours before temperature 

 could affect it. 1273 Furthermore, it was found that oxygen could affect the develop- 

 ment of the eye two or three days after temperature could affect the development of 

 the eye. 849 It became, as more and more agents were used, a little more ludicrous to 

 say that the gene was acting at this time, that time, or the other time. The effect of 

 the environment on the development of the organism may be related to the gene, but 

 usually it is not and certainly it need not be. Cause and effect are not so easily related. 



Dr. Burdette: I regret that we do not have more time to devote to the dissection 

 of these complexities. Dr. Wright, perhaps you wish to make a few concluding remarks 

 at this time, particularly with relation to evolution. 



Dr. Wright : I will not attempt to summarize in any detail what I said in my paper. 

 I wish merely to emphasize again that because of the prevalence of intermediate optima 

 in quantitative variability, and also of pleiotropy, multiple selective peaks are. to be 

 expected in any species in the virtually infinite field of possible sets of genie frequencies. 

 Each of these peaks tends to be closely related to an equilibrium point determined in 

 part by the pressures of recurrent mutation and immigration but primarily by mean 

 selective value. These equilibrium points have the property to which Lerner has 

 applied the term genetic homeostasis. After any slight shift, the system tends to 

 return to the same equilibrium. 



The selective peaks may be expected to differ greatly in adaptive value. The 

 evolutionary problem is the mechanism by which the species may work its way from 

 lower to higher peaks, necessarily somewhat against the pressure of selection in the 

 first stage. In a sexually reproducing species under given environmental conditions, 

 the only known mechanism is that in which some sort of random drift brings about 



