High impact information on dor

• Deep orange and carnation are two of the classic eye color genes in Drosophila [1].
• This locates the site of Dor function to fusion of Golgi-derived vesicles with the large Rab7-positive endocytic compartments [2].
• Overexpression of Dor in car1 mutant aggravates this defect, implicating Car in the removal of Dor from endosomes [2].
• This suggests that, in addition to an independent role in fusion with tubular lysosomes, the Sec1p homologue, Car, regulates Dor function [2].
• deep-orange and carnation define distinct stages in late endosomal biogenesis in Drosophila melanogaster [2].

Biological context of dor

• 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 [2].
• 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 [2].
• Mutations in hook (hk) and dor do not affect synaptic vesicle recycling, as assessed by electrophysiological analysis of synaptic transmission and behavioral studies of double mutants with shi(ts) mutations that alter vesicle recycling [3].
• Double mutants for dor and hk show a dor-like phenotype [3].
• Heterozygotes for lethal or viable dor alleles and the rearrangement T(1;2)dor(var7), which causes position effect variegation of dor, exhibit traits such as rough eyes, reduction of bristles on the thorax and scutellum and wavy wings [4].

Anatomical context of dor

• The 3.0-3.1 kb dor transcript was detected by Northern hybridization at all stages of development and is expressed in salivary glands of third instar larve [4].
• Hook, a negative regulator of endocytic trafficking, and Dor, a positive regulator of endocytic trafficking, are highly enriched at synapses, especially close to postsynaptic membranes [3].
• To study the function of endosomes at synapses we analyzed the localization and function of two Drosophila endosomal proteins, Hook and Deep orange (Dor), at the larval neuromuscular junction [3].
• Second, neither exogenous ecdysone nor overexpression of PTEN, a silencer of PI3K signaling, restored fusion of autophagosomes with lysosomes in the fat body of dor mutants [5].

Other interactions of dor

• However, hk and dor mutations alter the number of presynaptic varicosities (synapse size) in opposing ways [3].
• Two other loci dor and swi are situated some to the right of 2B5 [6].
• In addition, combinations of viable mutant alleles of some of these genes, such as carnation (car) combined with either light (lt) or deep-orange (dor) mutants, show lethal interactions [7].
• First, PI3K activity was not down-regulated correctly in dor larvae, which correlated with a decrease in ecdysone reporter activity [5].

References