RETINAL DEGENERATION IN RHODOPSIN STRUCTURAL GENE MUTANTS IN DROSOPHILA

DEBRA ANN SCARBOROUGH LEONARD, Purdue University

Abstract

Retinal morphology in flies bearing any one of several mutations in the ninaE gene, which encodes the species of opsin found in the Rl-6 class of photoreceptors, is described. Rl-6 rhabdomeres (organelles bearing the majority of rhodopsin) are initially present but degenerate in each ninaE mutant, suggesting that rhabdomere maintenance but not differentiation depends upon rhodopsin. Furthermore, the rate of degeneration is strongly correlated with the amount of rhodopsin in Rl-6 photoreceptors, suggesting that lesions in the ninaE gene cause degeneration. Rl-6 rhabdomere degeneration is light-independent, suggesting that it is not triggered by defective inputs from the phototransduction pathway. Axial complexes, which are major components of rhabdomeres in wild-type flies, are present in ninaE mutants, suggesting rhodopsin might not be a major component of these structures. Intracellular extensions of plasma and/or rhabdomere membranes, studded with bristly structures resembling coated pits, are abundant in Rl-6 cell bodies of severely affected ninaE mutants, and large, membrane-bound vacuoles also accumulate in such cells, suggesting that membrane turnover might be defective in these flies. Rhabdomeres of the less abundant photoreceptor clases are examined and often found to be disorganized in appearance, although they rarely, if ever, degenerate. Rhabdomeres also slowly degenerate, at least in the minor photoreceptor classes, in a ninaD mutant (in which rhodopsin contents are low because chromophore formation is defective; all opsin proteins are normal), thus suggesting that extreme reductions in rhodopsin content alone can cause rhabdomere degeneration.

Degree

Ph.D.

Subject Area

Genetics

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