Figure 6

Manipulation of PKD activity causes retina degeneration. A) Eyes of control flies have externally a smooth and regular appearance (left column). Tangential sections reveal the underlying, semi-crystalline architecture of the facets (center column). Seven photoreceptor cells can be distinguished by the centrally located rhabdomeres (arrow) that contain the light sensitive rhodopsin. Each facet is insulated by surrounding pigment cells that contain pigment granules (arrowhead). See enlargement in the right column. B) Overexpression of one or several copies PKD-SE^139-2 caused single black dots that have the size of a single facet (small arrow). Tangential sections reveal degeneration of the retina. The borders between ommatidia become blurred by many holes; also, fusion was observed. The pigment granules seem to clump and no longer encircle the rhabdomeres (arrowhead). The rhabdomeres are swollen and elongated; some are fragmented (arrow). Some rhabdomeres are absent and others degenerated. C) The defects remain largely unaltered when DIAP1 is overexpressed simultaneously, apart from a good rescue of the holes. D) Overexpression of dsPKD causes large black patches with a glossy surface (small arrow). Sections reveal massive amounts of cocci within the black patch (black arrowhead) underlying thinner lens (open arrow). Rhabdomeres are collapsed and degenerated (arrow); sporadic pigment granules can be seen (arrowhead). E) Concurrent overexpression of DIAP1 has little influence on the superficial appearance (arrow). However, the retina is somewhat more regular, which is reflected by the pigment granules that partly encircle the ommatidia (arrowhead). Moreover, rhabdomeres are well separated but many of them are degenerated (arrow). Genotypes are: A) wild type; B) gmr-Gal4/PKD-SE^139-2; C) UAS-DIAP1/+, gmr-Gal4/PKD-SE^139-2; D) gmr-Gal4/+, UAS-dsPKD^114-5 /+; D) UAS-DIAP1/+, gmr-Gal4/+, UAS-dsPKD^114-5 /+. Scale bar, 20 μm.