FOUNDATIONS FOR SEX 



27 



azteca. This genie "sex ratio"' sr lies in the 

 right limb of the X of races A and B of 

 D. pseudoobscura. Like the other cases 

 analyzed, males carrying sr have mostly 

 daughters and few sons regardless of the 

 genotypes of their mates. Structurally the 

 female sex ratio came through modification 

 of the development of the sex cells of the 

 male to give a majority of X-bearing sperm. 

 Cytologic study showed that in "sex ratio" 

 males the X underwent equational division 

 at each meiotic division, whereas the auto- 

 somes behaved normally. The Y chromo- 

 some lagged on the first spindle, remained 

 much condensed, and its spindle attachment 

 end was not attenuated. The Y chromosome 

 was not included in either telophase group 

 of the first meiotic division but was left be- 

 hind. It was sometimes noted in one of the 

 daughter cells where it formed a small nu- 

 cleus. Among 64 spermatocytes examined, 

 all had an X chromosome and none a Y 

 chromosome in their main nuclei. The mi- 

 cronuclei containing Y played no further 

 part in the division, became smaller and 

 exceedingly contracted. The final fate of the 

 micronuclci was uncertain, but there was no 

 indication that any spermatids died or were 

 abnormal. 



G. HIGH MALE SEX RATIO OF GENETIC ORIGIN 



In 1920, Thompson described a recessive 

 mutant in D. melanogaster which killed all 

 homozygous females but changed the male 

 phenotypes only slightly, the wings stand- 

 ing erect above the back. The locus of the 

 mutant was 38 in the X chromosome. This 

 mutant was a leader for a class in which the 

 genes affect only one sex but are innocuous 

 to the other. 



Bobbed-lethal, a sex-linked gene found 

 i)y Bridges, is a gene of this class but one in 

 which the mechanism of protection to the 

 other sex is known. It kills homozygous fe- 

 males but does not kill the males because of 

 the wild type allele which the males have in 

 their Y chromosomes. The presence of this 

 bobbed-lethal in a population consequently 

 leads to male ratios higher than wild type. 



A recessive gene in chromosome II, dis- 

 covered by Redfield (1926), caused the 

 early death of the majority of female zy- 

 gotes and led to a sex ratio of about 1 fe- 

 male to 5.5 males. The effect was trans- 



mitted througli both males and females. The 

 missing females may have died largely in 

 the egg stage although disproportionate 

 losses also occurred in the larvae and pupae. 

 The maternal effect was attributed to an 

 influence exerted by the chromosome con- 

 stitution of the mother on the eggs before 

 they left the mother's body. Because of this 

 maternal lethal, the families from these 

 mothers have the normal number of sons 

 but few or no daughters. 



A culture was observed by Gowen and 

 Nelson (1942) which yielded only male 

 progeny, 136 in all. Some of the male prog- 

 eny were able to transmit the male-produc- 

 ing characteristics to half of their daughters 

 without regard to the characteristics of the 

 mates to which they were bred. The in- 

 heritance was without phenotypic effect on 

 the males. When present in the hetero- 

 zygous condition in females, the female's 

 own phenotype gave no indication of the 

 gene's presence. The inheritance was sex 

 limited in that it affected only the eggs laid 

 by the mothers carrying it. In these eggs it 

 acted as a dominant lethal for the XX zy- 

 gotes. The gene was found located in the 3rd 

 chromosome between the marker genes for 

 hairy and for Dicheate at approximately 31. 

 The X eggs carrying the gene, Ne, died in the 

 egg stage at between 10 and 15 hours under 

 25°C. temperature. The gene was as ef- 

 fective in triploids as in diploids. One dose 

 of this gene in triploids caused them to have 

 only male progeny and male type intersexes. 

 The presence of this gene caused the elimi- 

 nation of any embryos with chromosomal 

 capacities for initiating and developing the 

 primary or secondary female sexual sys- 

 tems. Since the gene itself was heterozygous 

 in the female the meiotic divisions of the 

 eggs would cause the gene to pass into the 

 polar bodies as often as to remain in the 

 fertilization nucleus yet the lethal effects 

 are found in all eggs. The antagonism was 

 between the egg cytoplasm and the XX 

 fusion products. Supernumerary sperm of 

 the Y type were not sufficient to overcome 

 the lethal effects. An XY fertilization nu- 

 cleus was necessary for survival. 



This case has parallel features with that 

 observed by Sturtevant (1956) for a 3rd 

 chromosome gene that destroys individuals 

 bearing the first chromosome recessive gene 



