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).
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
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:
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
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