Ultrastructural effects of a suppressor mutation in Drosophila.

HE vermilion (U) mutants of Drosophila melanogaster are characterized by the absence of brown pigment in the eye and hence the mutant phenotype is a bright scarlet eye color. At the biochemical level, this phenotype is a result of the absence of tryptophan pyrrolase, the enzyme which catalyzes the conversion of tryptophan to formylkynurenine ( BAGLIONI 1960; KAUFMAN 1962; MARZLUF 1965). Tryptophan pyrrolase is localized in the anterior cells of the larval fat body, and accumulation of kynurenine in these cells may be detected long before the eye pigments are formed. Kynurenine displays a characteristic light blue fluorescence and its presence can be intracellularly localized by examination of freshly dissected fat body cells with the fluorescence microscope (RIZKI 1961). This method of examination has revealed that kynurenine appears in cytoplasmic globules in U+ fat cells near the end of larval life. Kynurenine autofluorescence is absent in the fat body cells of U mutant strains, although the globular site is present and receptive as demonstrated by in vitro incubation of U fat body cells in kynurenine solution, or by the feeding of kynurenine to U larvae. The latter experiments raised the possibility that intercellular diffusion of kynurenine may distort the analysis of cellular biosynthetic processes affected by the action of the U + locus. Therefore, the synthesis of genetic gynandromorphs containing mosaic U and U + fat body cells was used to demonstrate that the kynurenine visualized in a specific fat body cell at this stage of development is an endogenous product of that cell (RIZKI and RIZKI 1968). The kynurenine phenotype is thus an autonomous property of the U+ fat body cell and i t may be manipulated by several other nonallelic genes. Of particular interest is the modification introduced by the combination of the mutant genes suppressor-of-sable (su-s) and U. A number of U alleles are suppressed by the su-s gene (GREEN 1954) and verification of this suppression is indicated by the reappearance of kynurenine in the fat body cells as well as functional enzyme activity and normal eye color. On the other hand, some U alleles are not affected by the suppressor gene and the response of various suppressible alleles differs in the number of fat body cells which become engaged in kynurenine synthesis. For example, only the few cells limited to the dorsoanterior fat body overlying the salivary gland develop kynurenine in su2-s vSGf larvae, whereas the population of cells synthesizing kynurenine in su#-s v1 larvae is greater than that of U + larvae. Cells in specific regions of the fat body thus may be examined with respect to the genetic components involved in the elaboration