so 



CHAPTER 6 



FIGURE 6-9. Normal (right) and Creeper (left) roosters. (Courtesy of L. C. 

 Dunn; reprinted by permission of McGraw-Hill Book Co., Inc., from Study 

 Guide and Workbook for Genetics by I. H. Herskowitz. Copyright, 1960.) 



Creeper: normal chicks; Creepers crossed 

 with Creepers give, in the adult stage, 

 775:388 as Creeper: normal, a result which 

 is considered an excellent fit to a 2: 1 ratio. 

 It is reasonable to suppose, therefore, that 

 Creeper is heterozygous for a single pair of 

 segregating genes, in which the Creeper gene, 

 Cp, is dominant to its normal allele, +. 

 The 2 : 1 ratio is taken to indicate that the 

 mutant homozygote, Cp Cp, is lethal. The 

 possibility that Cp acts as a recessive lethal 

 is supported by a comparison of the survival 

 frequency of embryos having normal parents 

 with that of embryos having parents both of 

 which are Creeper. It is found that about 

 25% more embryos die within three days 

 of incubation in the latter than in the former 

 case. 



What is the developmental, phenogenetic 

 basis for Cp Cp, which acts as a recessive 

 lethal; Cp +, which produces Creeper; and 

 -| — |-, which produces normal? Although 

 Cp Cp usually dies within three days of in- 

 cubation, on rare occasions it survives 19 

 days, about the time of hatching from the 

 shell. Such a rare Creeper homozygote is 

 shown at the left of Figure 6-10 (the com- 

 parable normal individual is at the right) 



and possesses the following syndrome of 

 malformations: the eyes are split, smaller 

 than normal, and have no eyelids; the head 

 is misshapen, and the body is smaller; the 

 skeleton is not ossified and — as seen on top 

 of the black paper used as background in 

 the figure — only the digits of the limbs are 

 well formed. 



A study of Cp -j- development shows that, 

 at seven days of incubation, the leg buds 

 are shorter than in normal embryos. This 

 morphological manifestation of Cp action 

 must be based upon events occurring earlier 

 in development, for at 48 hours of incuba- 

 tion (Figure 6-11), a Cp -\- embryo (left) 

 is smaller, less developed, and does not have 

 the head flexure already present in a H — (- 

 embryo (right). In fact, differences like 

 this can be seen even twelve hours earlier, 

 i.e., at 36 hours of incubation. 



In both the homozygote and heterozygote 

 for Cp, the differentiation of cartilage has 

 been disturbed. The Cp -+- individual has 

 the disease called chondrodystrophy (or 

 achondroplasia) and the CpCp individual 

 has the cartilage disease, phocomelia (see 

 p. 4). Both diseases were recognized in 

 human families more than a hundred years 



