Section 4 — Gene action 



preparation inactivated the wild type enzyme 

 whereas an anti-ry 2 antibody preparation was 

 ineffective. A discussion of these data will be 

 presented. 



4.29. A Possible Explanation for Some of the Differ- 

 ences between Drosophila Mutants lacking 

 Xanthine Dehydrogenase. Edward Glassman 

 (Chapel Hill, U.S.A.). 



Both the maroon-like {ma-1) and the rosy (ry) 

 eye color mutants of Drosophila melanogaster 

 lack detectable amounts of the enzyme, xanthine 

 dehydrogenase. However, when extracts of these 

 two mutants are mixed together and incubated 

 for 90 min at 30°C, xanthine dehydrogenase 

 activity is produced in the absence of protein 

 synthesis. W It is postulated that there is a 

 /Ha-7 + -complementing substance in ry extracts 

 and a rv+-complementing substance in ma-1 

 extracts, and that these complementing substan- 

 ces interact to produce active xanthine dehydro- 

 genase. Preincubation of each of the mutant 

 extracts at various temperatures has shown that 

 the /no-/+-substance is very much more stable to 

 mild heat treatment (35° to 50°C) than is the 

 0>+-substance. If this difference in stability 

 occurs in vivo, it would explain some of the differ- 

 ences between the ma-1 and ry mutants. Thus, 

 there is no maternal effect at the ry locus be- 

 cause the ry+-substance is too unstable to persiss 

 in the egg. (2 ) In addition, the difference in effectt 

 of gene dosage at these two loci can also be ex- 

 plained by the relative instability of the /-.^-sub- 

 stance. The more stable wa-/+-substance will 

 pile up in the cell to such an extent, that even if 

 its level drops in response to lower doses of 

 ma-l+, it will still be in excess, and no change in 

 xanthine dehydrogenase activity will occur. Thus 

 only the ry locus has a gene dosage effect on the 

 enzyme activity; the ma-1 locus does not. 



This research was supported in part by a 

 research grant (GM 08202-03) from the National 

 Institutes of Health. 



1. Proc. Nat. Acad. Sci. 48, 1491. 



2. Proc. Nat. Acad. Sci. 48, 1712. 



4.30. Gene Control of Eye Pigments in Mormoniella. 



G. B. Saul (Hanover, U.S.A.). 



Wild type eye color results from the presence 

 of at least three pigments separable by chromato- 

 graphy. Two of these, a yellow and a red pig- 

 ment, are present in scarlet-eyed mutants but not 



in a black-eyed mutant type; the other, a purple 

 pigment, is absent from scarlet-eyed wasps but 

 present in the black-eyed type. Spectrophoto- 

 metry and chemical tests indicate that the yellow 

 and red pigments may be pteridines; the nature 

 of the purple pigment is unknown, but it does not 

 appear to resemble the brown ommochrome of 

 Drosophila. 



Three loci contain mutations for black eye 

 color. Mutants of one of these contain only 

 purple pigment and accumulate isoxanthopterin 

 and 2-amino-4-hydroxypterine; the second group 

 of mutants contain all eye pigments of wild type 

 and do not accumulate the pteridines; and wasps 

 containing mutations at the third locus contain 

 all eye pigments of wild type and also accumulate 

 the pteridines. 



Scarlet-eyed mutants result from changes at 

 any of four known loci. They cannot be distin- 

 guished from each other by color or chromato- 

 graphy, but have separable phenotypes when also 

 containing mutant genes for black eye color. 



4.31 . The Genetics of Esterases in Drosophila melano- 

 gaster. Theodore R. F. Wright (Baltimore 

 U.S.A.). 



Ogita W reports the existence of a genetic 

 factor (ali ) on the 3rd chromosome which lowers 

 the esterase activity (methyl butyrate used as the 

 substrate) of homogenates of whole adult flies. 

 Homogenates from ali-/ali~ individuals have 

 only 15 per cent as much activity as homogenates 

 from ali+/ali+ individuals. Heterozygotes, ali+/ 

 ali~, have intermediate activities; approximately 

 55 per cent of ali+/ali+. Wright < 2 ) reports that 

 two codominant alleles which control the struc- 

 ture of an esterase designated as Esterase 6 are 

 located at 36.8 ± on the 3rd chromosome. 

 Starch gel electrophoresis of homogenates show 

 that homozygotes for the allele, Est 6 F , produce 

 a form of Esterase 6 which migrates faster then 

 that produced by homozygotes for the other 

 allele, Est 6 s . The heterozygote, Est 6 F /Est 6 s , 

 produces both fast and slow forms. 



Because both of the above genetic systems are 

 concerned with esterase production and because 

 both are located on the 3rd chromosome, it be- 

 came desirable to investigate whether or not the 

 two systems are interrelated. Three of Ogita's 

 strains, one ali+/ali+ and two ali-/ali-, are homo- 

 zygous for Est 6 s . Using p-nitrophenyl acetate 

 as a substrate, the total esterase activities of the 

 Est 6 F and Est 6 s strains (which are equal to one 

 another) are comparable to that of the ali+/ali + 

 strain. These data are not conclusive, however, 

 and data comparing not total esterase activities, 



46 



