Abstract:The fly visual system has served for decades as a model for receptor spectral multiplicity and vitamin A utilization. A diverse armamentarium of structural techniques has dovetailed with convenient electrophysiology, photochemistry, genetics, and molecular biology in Drosophila to facilitate recent progress, which is reviewed here. New data are also presented. Ultrastructure of retinula cells of carotenoid‐deprived flies shows that organelles associated with protein biosynthesis, i.e., rough endoplasmic reticu… Show more
“…In addition, the overall levels of Rhodopsin as well as rhabdomeric Rh1 (revealed by immuno-EM) are reduced ( Huber et al, 1994 ; Sapp et al, 1991 ). We confirmed the development of thinner rhabdomeres ( Lee et al, 1996 ) in wild-type PRCs upon carotenoid depletion ( Fig. 5 G vs. 5 E ).…”
Apical domains of epithelial cells often undergo dramatic changes during morphogenesis to form specialized structures, such as microvilli. Here, we addressed the role of lipids during morphogenesis of the rhabdomere, the microvilli-based photosensitive organelle of Drosophila photoreceptor cells. Shotgun lipidomics analysis performed on mutant alleles of the polarity regulator crumbs, exhibiting varying rhabdomeric growth defects, revealed a correlation between increased abundance of hydroxylated sphingolipids and abnormal rhabdomeric growth. This could be attributed to an up-regulation of fatty acid hydroxylase transcription. Indeed, direct genetic perturbation of the hydroxylated sphingolipid metabolism modulated rhabdomere growth in a crumbs mutant background. One of the pathways targeted by sphingolipid metabolism turned out to be the secretory route of newly synthesized Rhodopsin, a major rhabdomeric protein. In particular, altered biosynthesis of hydroxylated sphingolipids impaired apical trafficking via Rab11, and thus apical membrane growth. The intersection of lipid metabolic pathways with apical domain growth provides a new facet to our understanding of apical growth during morphogenesis.
“…In addition, the overall levels of Rhodopsin as well as rhabdomeric Rh1 (revealed by immuno-EM) are reduced ( Huber et al, 1994 ; Sapp et al, 1991 ). We confirmed the development of thinner rhabdomeres ( Lee et al, 1996 ) in wild-type PRCs upon carotenoid depletion ( Fig. 5 G vs. 5 E ).…”
Apical domains of epithelial cells often undergo dramatic changes during morphogenesis to form specialized structures, such as microvilli. Here, we addressed the role of lipids during morphogenesis of the rhabdomere, the microvilli-based photosensitive organelle of Drosophila photoreceptor cells. Shotgun lipidomics analysis performed on mutant alleles of the polarity regulator crumbs, exhibiting varying rhabdomeric growth defects, revealed a correlation between increased abundance of hydroxylated sphingolipids and abnormal rhabdomeric growth. This could be attributed to an up-regulation of fatty acid hydroxylase transcription. Indeed, direct genetic perturbation of the hydroxylated sphingolipid metabolism modulated rhabdomere growth in a crumbs mutant background. One of the pathways targeted by sphingolipid metabolism turned out to be the secretory route of newly synthesized Rhodopsin, a major rhabdomeric protein. In particular, altered biosynthesis of hydroxylated sphingolipids impaired apical trafficking via Rab11, and thus apical membrane growth. The intersection of lipid metabolic pathways with apical domain growth provides a new facet to our understanding of apical growth during morphogenesis.
“…Therefore, photoreceptor cells increase their quantum efficiency by forming multilayered stacks of membranes that are tightly packed with photosensitive rhodopsin molecules. This functional cytoarchitecture can likewise be observed in vertebrate [86] and invertebrate eyes [87], where stacks of membrane discs or rhabdomeric microvilli ensure high quantum efficiency of each photosensitive cell. In the case of olfactory sensory neurons, however, the situation is slightly different.…”
Smell is often regarded as an ancillary perception in primates, who seem so dominated by their sense of vision. In this paper, we will portray some aspects of the significance of olfaction to human life and speculate on what evolutionary factors contribute to keeping it alive. We then outline the functional architecture of olfactory sensory neurons and their signal transduction pathways, which are the primary detectors that render olfactory perception possible. Throughout the phylogenetic tree, olfactory neurons, at their apical tip, are either decorated with cilia or with microvilli. The significance of this dichotomy is unknown. It is generally assumed that mammalian olfactory neurons are of the ciliary type only. The existance of so-called olfactory microvillar cells in mammals, however, is well documented, but their nature remains unclear and their function orphaned. This paper discusses the possibility, that in the main olfactory epithelium of mammals ciliated and microvillar sensory cells exist concurrently. We review evidence related to this hypothesis and ask, what function olfactory microvillar cells might have and what signalling mechanisms they use.
“…Whereas the fluorescence of Drosophila rhodopsin is negligible, the metarhodopsin strongly fluoresces, with a high emission in the red wavelength range (Stavenga 1983 ; Stavenga et al 1984 ). The fluorescence measurements are preferably applied in white-eyed mutants and are performed with a microspectrophotometer where a diaphragm isolates the fluorescence from the deep pseudopupil (Lee et al 1996 ; Stark and Thomas 2004 ). Other pigments than Rh1 metarhodopsin contribute to the emission signal, especially with blue excitation light.…”
We have simultaneously measured the electroretinogram (ERG) and the metarhodopsin content via fluorescence in white-eyed, wild-type Drosophila and the arrestin2 hypomorphic mutant (w -;arr2 3 ) at a range of stimulus wavelengths and intensities. Photoreceptor response amplitude and termination (transition between full repolarization and prolonged depolarizing afterpotential, PDA) were related to visual pigment conversions and arrestin concentration. The data were implemented in a kinetic model of the rhodopsin-arrestin cycle, allowing us to estimate the active metarhodopsin concentration as a function of effective light intensity and arrestin concentration. Arrestin reduction in the mutant modestly increased the light sensitivity and decreased the photoreceptor dynamic range. Compared to the wild type, in the mutant the transition between full repolarization and PDA occurred at a lower metarhodopsin fraction and was more abrupt. We developed a steady-state stochastic model to interpret the dependence of the PDA on effective light intensity and arrestin content and to help deduce the arrestin to rhodopsin ratio from the sensitivity and PDA data. The feasibility of different experimental methods for the estimation of arrestin content from ERG and PDA is discussed.
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