24 PHYSIOLOGICAL GENETICS 



they go, may be interpreted <>u the basis of different rates of 

 reaction. 



A second group includes cases that are rather complex in 

 detail, because the mutant form exhibits complicated patho- 

 logical conditions which are difficult to describe in simple terms, 

 although very thorough work has been done. This group con- 

 tains mosl of the recent work on mammals and birds. The 

 abnormalities arc caused by either recessive or dominant mutant 

 genes, the latter being sometimes lethal in homozygous condition. 

 There i< the work of Little and Bagg (1929), Bonnevie (1934), and 

 Plagens (1933) on a recessive mutation produced by X-ray 

 t nat ment by Little and Bagg. The abnormality is very diversi- 

 fied, affecting many different organs, especially eye and foot. It 

 seems that all these changes are the consequence of a blood 

 extravasate occurring in the neck of embryos 7 to 8 mm. in 

 length (Bonnevie). The blebs move with further development 

 to different places where they obstruct mechanically the processes 

 of development. We may not, in this case, speak properly of 

 changes in development produced by the mutant gene. It 

 actually produces only one effect: In young embryos, fluid from 

 the medullary tube is expelled through the foramen anterius in 

 abnormal quantity, and the blebs thus formed harm the develop- 

 mental processes wherever they become situated. 



In some of the other abnormalities, however, actual develop- 

 mental processes are changed by the mutant gene. The develop- 

 ment of the short-tailed mutation of the mouse, found by 

 Dobrovolskaja (1928) as a dominant mutation, lethal in homozy- 

 gous state, has been studied by Chesley (1935). (The morphology 

 of the mutant is carefully analyzed by Kobozieff, 1936). The 

 homozygous embryos show, as far as can be determined, normal 

 development up to the somite state. Then a considerable 

 degeneration of tissue sets in, as indicated by the appearance of 

 chromatic granules, in the posterior part of the embryo. This 

 results in the absence of notochord, medulla, and somites and 

 leads to death of the germs (10?^ days after insemination). The 

 facts seem to point out that the degeneration process begins in 

 the primitive streak and therefore affects all the descendant 

 parts (and the induced differentiation) of this region. It is 

 obvious how much this case resembles the case of the vestigial 

 wing in its general features, which will be reported below. In 



