Considering how bad the retina looks optically, in the deep pseudopupil and with optical neutralization of the cornea (see this text), it is astounding how many untrastructural features of the visual system in eight day post-eclosion adults are close to normal. Retinula cells appear healthy and have normal nuclei and mitochondria (1)(3). They are connected to their neighboring retinula cells with the appropriate belt desmosomes (2)(3). Rhabdomeres have the customary submicrovillar cisternae (3). Within microvilli, there is the usual electron dense rod (3). Also retinula cells have normal intraretinular pigment granules (5) and rhabdomere caps (6). The intraretinular pigment granules are know to migrate toward the rhabdomere in the light, and their position is indicative that the cell was responding to light at the time of fixation (5).

Axons from the retina proceed through the basement membrane to the first optic neuropil, the lamina ganglionaris, where the R1-6 terminals form into the appropriate synaptic glomeruli, optic cartridges (7, control left, GGA kd right, bottom of figure). The reason this was considered to be important was that, in rdgB (which has light-induced retinal degeneration), R1-6 terminals in the optic cartridges showed gross degeneration under the minimal dim red light conditions sufficient for dissection forfixation (Stark & Sapp, 1989), well before the retinula cells in the retina fill with a dense reticulum and lipid droplets (Stark & Carlson, 1982). Close examination reveals the membrane specializations that characterize functional synapses, the T-bars (8).

(figure, knockdown left, control right) It is tempting to speculate that the rich investment of membrane circles in the retinula cell cytoplasm near the rhabdomere is a characteristic feature of the GGA kd; however, the control also shows these structures, and it is not realistic to compare them quantitatively. Such circles were posited as the vehicles to carry rhodopsin and/or membrane to rhabdomeres during vitamin A replacement (Stark et al, 1988); also they were plentiful in ora (outer rhabdomeres absent) where there were no rhabdomeres to receive membrane intended for rhabdomeres (Stark & Sapp, 1987) and after retinoic acid feeding (Lee et al, 1996). Importantly, they fill the retinula cell cytoplasm in Rab11 mutant cells that lack rhodopsin transport to the rhabdomeres (Satoh et al, 2005). Such vesicles also fill the cytoplasm in Drosophila Rip11 (Rab11 interacting protein) mutants (Li et al, 2007).

[The knockdown figure (left) shows a split R7 rhabdomere and several gross abnormalities at the 11 and 2 o'clock positions, presumably in secondary pigment cells.]

This list of healthy features focuses our attention on the most striking abnormalities: the size, orientation and number of rhabdomeres in each ommatidium are irregular (2); also there are gaps between ommatidia (9); some gaps may represent fused or fragmented ommatidia, others may have resulted from damage during tissue preparation for fixation. Upon examination of ommatidia with too many rhabdomeres, the retinula cell count is usually correct; thus retinula cells often have too many rhabdomeres (2) (4). While autophagic bodies, large endosomes, abnormal lysosome-related bodies, or disrupted biosynthetic machinery (Golgi apparatus or rough endoplasmic reticulum) might have been expected, no striking alterations from control were present.


Lee RD, Thomas CF, Marietta RG, Stark WS (1996) Vitamin A, visual pigments and visual receptors in Drosophila. Micros Res Tech 35: 418-430

Li BX, Satoh AK, Ready DF (2007) Myosin V, Rab11, and dRip11 direct apical secretion and cellular morphogenesis in developing Drosophila photoreceptors. J Cell Biol 177: 659-669

Satoh AK, O'Tousa JE, Ozaki K, Ready DF (2005) Rab11 mediates post-Golgi trafficking of rhodopsin to the photosensitive apical membrane of Drosophila photoreceptors. Development 132(7): 1487-1497

Stark WS, Carlson SD (1982) Ultrastructural pathology of the compound eye and optic neuropiles of the retinal degeneration mutant (w rdgBKS222) Drosophila melanogaster. Cell Tissue Res 225: 11-22

Stark WS, Sapp RJ (1987) Ultrastructure of the retina of Drosophila melanogaster: The mutant ora (outer rhabdomeres absent) and its inhibition of degeneration in rdgB (retinal degeneration-B). J Neurogenet 4: 227-240

Stark WS, Sapp RJ (1989) Retinal degeneration and photoreceptor maintenance in Drosophila: rdgB and its interaction with other mutants. In Inherited and Environmentally Induced Retinal Degenerations, LaVail MM, Anderson RE, Hollyfield JG (eds), pp 467-489. New York: Liss

Stark WS, Sapp RJ, Schilly D (1988) Rhabdomere turnover and rhodopsin cycle: maintenance of retinula cells in Drosophila melanogaster. J Neurocytol 17: 499-509

Last revised 6/15/10

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