deep-orange and carnation define distinct stages in late endosomal biogenesis in Drosophila melanogaster

Endosomal degradation is severely impaired in primary hemocytes from larvae of eye color mutants of Drosophila. Using high resolution imaging and immunofluorescence microscopy in these cells, products of eye color genes, deep-orange (dor) and carnation (car), are localized to large multivesicular Rab7-positive late endosomes containing Golgi-derived enzymes. These structures mature into small sized Dor-negative, Car-positive structures, which subsequently fuse to form tubular lysosomes. Defective endosomal degradation in mutant alleles of dor results from a failure of Golgi-derived vesicles to fuse with morphologically arrested Rab7-positive large sized endosomes, which are, however, normally acidified and mature with wild-type kinetics. This locates the site of Dor function to fusion of Golgi-derived vesicles with the large Rab7-positive endocytic compartments. In contrast, endosomal degradation is not considerably affected in car1 mutant; fusion of Golgi-derived vesicles and maturation of large sized endosomes is normal. However, removal of Dor from small sized Car-positive endosomes is slowed, and subsequent fusion with tubular lysosomes is abolished. Overexpression of Dor in car1 mutant aggravates this defect, implicating Car in the removal of Dor from endosomes. This suggests that, in addition to an independent role in fusion with tubular lysosomes, the Sec1p homologue, Car, regulates Dor function.

Variation in the pteridine content in the heads of tsetse flies (Diptera: Glossinidae: Glossina Wiedemann): evidence for genetic control

The pteridine content of the head capsule of teneral flies from 11 genetically selected lines (including eye-color mutants) of Glossina morsitans morsitans Westwood and Glossina palpalis palpalis Robineau-Desvoidy was examined using fluorescence spectroscopy. Wild-type G. p. palpalis had a greater pteridine content than did wild-type G. m. morsitans. Within G. m. morsitans there was a 25% variation in fluorescence values between genetic lines. Wild-type G. p. palpalis had the same pteridine content as brick mutants but more than tan mutants; in G. m. morsitans the salmon mutants had a higher pteridine content than did wild-type flies. Pteridine content did not account for the difference in eye color between male and female brick mutants. Accumulation of pteridines was not influenced by genotype in young flies, but in older flies salmon mutants accumulated pteridines more rapidly than did wild-type flies. Young flies, both wild type and salmon, accumulated pteridines more rapidly than did old flies. The results of the analysis of head capsule fluorescence in males from the parental lines and F1 and F2 generations of reciprocal crosses of the G. m. morsitans lines with the highest and lowest pteridine contents revealed that genetic control of pteridine content lies on the X chromosome and on one autosome.

Genetics of Glossina palpalis palpalis: designation of linkage groups and the mapping of eight biochemical and visible marker genes

The loci for three enzymes (hexokinase, phosphoglucomutase, and testicular esterase) and two eye-color mutants (brick and tan) are mapped on the X chromosome of Glossina palpalis palpalis. The loci occur in the order brick Hex (tan/Pgm) Est-t, with a recombination frequency of approximately 78% between the outer two loci. The locus for octanol dehydrogenase is located in linkage group II and the loci for malate dehydrogenase and phosphoglucose isomerase are separated by a recombination frequency of about 42.5% in linkage group III. Intrachromosomal recombination occurs at a much lower frequency in males than in females. The distribution of five biochemical marker genes in the linkage groups of G. p. palpalis is markedly different from that found in other higher flies.Key words: tsetse, Glossina palpalis palpalis, linkage map.