Some mutations affecting neural or muscular tissues alter the physiological components of the electroretinogram in Drosophila

Abstract

Mutants displaying generalized behavioral defects and one mutant having an enzyme deficiency were examined for electroretinogram (ERG) defects. Mutations in nine genes were examined that cause ERG defects. Two, parats4 and slrpD, cause reversibly temperature dependent loss of the off-transients in the ERG. stnC and Tyr-2 cause loss of the on and off-transients. The transient defect in Tyr-2 mapped close to a site shown to affect tyrosinase activity in this strain. Mutations bas, rex and sesD delay recovery from the prolonged depolarization afterpotential. The visual defects of mutations elavjl and nbAEE171 are not complemented by lethal mutations, which, presumably, affect other tissues.