100 



It has therefore been concluded that 

 the 25 per cent missing from the lit- 

 ters, the 25 per cent of disintegrating 

 embryos, and the 25 per cent of ex- 

 pected pure yellows are the same. The 

 intrauterine death of this class has 

 been supposed to be due to a recessive 

 lethal gene which when received from 

 both parents causes the death of the 

 resulting zygote or individual. In 

 every case this lethal gene has been 

 transmitted with the gene for yellow. 

 It may be either completely linked or 

 identical with the gene for yellow. At 

 any rate it is present at the same locus 

 with the gene which determines yel- 

 low, and any individual which receives 

 yellow from both parents receives 

 likewise the lethal gene from both 

 parents and is doomed to death before 

 birth. As to why this combination of 

 two lethal genes is fatal we are still in 

 the dark. 



This yellow gene and the lethal as- 

 sociated with it are known only in 

 house mice,^ and the restricted yellow 

 of the other species has not been re- 

 ported in house mice. They are prob- 

 ably not homologous variations in 

 spite of their similarity in appearance. 

 The "yellow" varieties of rats are not 

 really to be classified with other yel- 

 low rodents since they are actually 

 "agoutis," differentiated from the wild 

 gray by the pink-eye gene (to which 

 we have referred) or by the very 

 similar red-eye gene which act selec- 

 tively on the melanic pigments to re- 

 duce rather than restrict them. 



WHITE-SPOTTING 



Almost as common as albinism 

 among rodents is the spotting of cer- 



* Several other factors may modify the 

 appearance of yellow in mice; for instance, 

 certain darkening factors in the presence of 

 the yellow gene produce the black-and-tan 

 and sable varieties of mice, while intensify- 

 ing factors in the presence of yellow produce 

 the brighter orange or red varieties. 



DUNN 



tain portions of the coat with white. 

 The white areas are as devoid of pig- 

 ment as in albinos but here the likeness 

 ends. Genetically white-spotting and 

 albinism are distinct and contrary to 

 the popular belief are not quantita- 

 tively but qualitatively unlike. Albi- 

 nism is fundamentally the loss or 

 change of a factor for the development 

 of a peroxidase essential to the produc- 

 tion of any pigment (cf. Wright '17) 

 and its effects are of a general nature 

 throughout the pelt and eyes. Spot- 

 ting appears to be a change in a factor 

 governing the distribution of the pig- 

 ments in the pelage. When pigmenta- 

 tion is present all over the pelt the 

 condition is known as self or not- 

 spotted. Spotting is inherited inde- 

 pendently of albinism, since certain 

 albinos crossed with spotted animals 

 throw only selfs, while other albinos 

 derived from white-spotted colored 

 stocks have given spotted offspring. 

 An albino may therefore be genetically 

 either self or spotted although unable 

 to give evidence of this condition ex- 

 cept in its offspring by a colored ani- 

 mal which supplies the gene for the 

 development of color. 



On the grounds of its inheritance 

 white-spotting in rodents may be clas- 

 sified in three categories. The first of 

 these is piebald or Dutch spotting, ap- 

 parently due to a gene recessive to 

 self coloration and probably inde- 

 pendent of other coat color unit char- 

 acters. It may thence be present with 

 albinism, yellow, pink-eye, agouti or 

 black (see below). Piebald animals 

 may be characterized by a tv^pical 

 localization of the spotting in a belt 

 or collar as in belted mice or Dutch 

 rabbits; the spotting may be confined 

 to the face ("white-face" mice), or it 

 may be distributed in a fairly uniform 

 dorsal pattern as in hooded rats.^ On 



"^ A hooded Microtus has been noticed in 

 the Museum of Comparative Zoology at Har- 

 vard University. 



