THE MUTATED GENE 25 



the heterozygote, the developmental processes involved in pro- 

 ducing the short-tailed type are of the same order. I'm abnor- 

 mal development, affecting primarily the notochord, begins al 

 a much Later stage and therefore affects only (or mostly) the tail. 

 Here, then, the controlling factor is also the different time of 

 onsel of the degenerative process, as in the vestigial case. 



The number of reports in this field of research is constantly 

 increasing, and the facts appear rather variable, though in general 

 they may be described in a similar way. Sere arc a few more 

 examples: van Assen (1930) finds thai genetic vertebral ankylosis 



is based upon th currence of a fold in early development which 



causes a shift in the time relations of the developmental processes. 

 I >avid (1932) studied hairlessness in different types and finds it to 

 be caused by very different processes in the different forms. 

 Sometimes development proceeds normally, but at a definite 

 point cysts are formed which de-troy the follicle. In still other 

 forms the follicle degenerates. Bonnevie (1936a) extended her 

 studies to the destruction of the labyrinth in Dunn's "shaker- 

 short" mice. In the development of these waltzing mice, the 

 labyrinth develops first normally up to the eleventh day. Only. 

 then does abnormal differentiation set in. It is caused by abnor- 

 mal development of the myelencephalon, combined with a 

 collapse of its ventricle. A consequence is that the auditory 

 vesicle is not innervated and doe- not continue normal differen- 

 tiation. We might finally mention in this connection the radium- 

 induced mutant abnormalities of Antirrhinum, which Stein (1932- 

 1935) produced. Here, also, a primary tissue destruction of a 

 cancerous type leads to formative changes and abnormalities, 

 though not strictly comparable to the case- in animal.-. 



In the fowl, two comparable abnormalities have been studied. 

 There is the creeper fowl, showing a general achondroplasia of 

 the bone- in heterozygous condition, the homozygous mutant 

 being lethal il.andauer and Dunn. 1930//). The morphology 

 ami physiology of this mutant have been studied most thoroughly 

 by Landauer in a large series of paper-, and we know more about 

 the effects of the creeper gene than about any other comparable 

 case. We -hall report the case and other similar one- in another 



chapter i -ee paije 214). 



Another comparable abnormality, caused by a dominant factor 



(viable when homozygous), is the rumple-- fowl, in which the 



