D.— ZOOLOGY loi 



of the mutant white-eyed stocks as compared with that of wildtype 

 Drosophila melanogaster and when, in the following year, Hyde, using 

 wildtype and truncate flies produced evidence which seemed to show that 

 duration of life had a genetic basis. In 1916 Morgan and Bridges listed 

 all the known mutants in the X-chromosome of Drosophila melanogaster 

 and noted for many of them their effect upon the duration of life. They 

 found that certain mutant genes very effectively reduce the viability of 

 the males and alter the secondary sex ratio and discovered a number of 

 sex-linked ' lethal ' genes which caused the death of all males carrying 

 them. Later Pearl and Parker (1921) proceeded to demonstrate the 

 constancy of definite degrees of mean longevity of inbred stocks of 

 Drosophila. They found, for example, that their ' Old Falmouth ' wild- 

 type males had at emergence an expectation of life of 41 -o days, whereas 

 quintuple males with 5 mutant genes had one of only 14-2 days. Crosses 

 between the two stocks were made by Pearl, Parker and Gonzalez (1923), 

 and in the F.^ definite evidence of segregation presented itself. Gonzalez 

 (1923) further studied the mean duration of life of strains of Drosophila 

 possessing i, 2, 3, 4 and 5 of these mutant genes, and ascertained that in 

 so far as their effect on duration of life was concerned, the individual 

 mutants behaved as units. 



Since this time a great mass of information concerning these matters 

 has been accumulated, and it is clear that these lethals exist in considerable 

 numbers in such animal and plant stocks that have been subjected to 

 genetical experimentation. They are not vague abstractions invoked 

 by the diagnostically destitute to explain away a mortality that they cannot 

 comprehend : they are genes which can be mapped and which have an effect 

 upon the secondary sex ratio that can be predicted. They can be in- 

 corporated into and rejected from a genotype at will and in this way the 

 dimensions of a secondary sex ratio can, within limits, be experimentally 

 controlled. Their presence and wide distribution in wild populations 

 have been amply demonstrated, and no doubts remain that they are 

 responsible, in part at least, for the higher mortality of the heterogametic 

 sex, both pre- and post-natally. 



But there are genetic differences between the sexes which are sex- 

 limited, not sex-linked. Levit (1935) has presented a very consider- 

 able body of evidence which shows that many defects and derangements 

 in man, formerly regarded as recessives, are partial irregular dominants, 

 and that many of these are more often and more completely expressed 

 in the male than in the female. Furthermore, he has shown that many of 

 these characters which previously had been classified as sex-linked are in 

 reality sex-limited, being expressed only in the male. He explains the 

 greater manifestation of heterozygous genes, corresponding to defects, in 

 the male, on the ground that in man selection is less intense among males 

 than among females so that such genes would tend to accumulate in the 

 male as would also genes causing sex-limitation. From an examination 

 of the sex ratio among the relatives of the father and mother Levit has been 

 led to the conclusion that few of the male deaths at or before birth are 

 due to sex-linked lethals. From this it would appear that though sex- 

 linked lethals are certainly responsible for some of the differences in male 



