1989
DOI: 10.3109/01677068909167263
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Some Mutations Affecting Neural or Muscular Tissues Alter the Physiological Components of the Electroretinogram inDrosophila

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 fro… Show more

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Cited by 20 publications
(16 citation statements)
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“…These synaptic effects, along with the bang-sensitive phenotype in all 4. mutations studied here, are suppressed by the mutation nap ts (no action potential, temperature-sensitive), which reduces the number of Na + channels (Ganetzky and Wu 1982a;Wu and Ganetzky 1992). Electroretinograms in a bas mutant showed delayed recovery from the prolonged depolarizing after-potential (Homyk and Pye 1989), suggesting effects upon the primary photoreceptors. The tko and eas genes have been sequenced and inferred by homology to encode a mitochondrial ribosomal protein and a choline kinase, respectively (Roydon et al 1987;Pavlidis et al 1993).…”
Section: Introductionmentioning
confidence: 99%
“…These synaptic effects, along with the bang-sensitive phenotype in all 4. mutations studied here, are suppressed by the mutation nap ts (no action potential, temperature-sensitive), which reduces the number of Na + channels (Ganetzky and Wu 1982a;Wu and Ganetzky 1992). Electroretinograms in a bas mutant showed delayed recovery from the prolonged depolarizing after-potential (Homyk and Pye 1989), suggesting effects upon the primary photoreceptors. The tko and eas genes have been sequenced and inferred by homology to encode a mitochondrial ribosomal protein and a choline kinase, respectively (Roydon et al 1987;Pavlidis et al 1993).…”
Section: Introductionmentioning
confidence: 99%
“…The cac gene was recently cloned and shown to encode Review Article a voltage-gated calcium channel h1 subunit (Dmca1A; [67]). The cac mutations were found to be allelic to nightblind-A (nbA), a series of mutations that are defective in visually mediated behaviors [68,69], accompanied by aberrant electroretinographic (ERG) responses to light stimuli [70]. Although cac s homozygotes do not exhibit any detectable phenotype in terms of visuallyguided behavior or ERG pattern, the cac s mutants exhibit visual abnormalities when tested in heteroallelic combinations: cac s /cac L − 6 flies performed poorly in Y-tube phototaxis, and the ERG of cac s /cac L10 flies showed a reduced on-transient followed by an aberrant undershoot [65].…”
Section: Motor Controlmentioning
confidence: 99%
“…The latter explanation turned out to be the case: Shankar Kulkarni and I showed in 1987 that the etiology of abnormal courtship song in this strain maps to a different region of the region of the relevant (X) chromosome-one that was readily separable from the factor which makes the males slow to achieve copulation. Later, it turned out that the cacophony gene does act pleiotropically, as revealed by the effects of other independently isolated alleles (e.g., Homyk & Pye, 1989;Smith et al, 1998;Dellinger et al, 2000;Chan et al, 2002), although the original mutation at the locus is much more limited in its behavioral effects.…”
Section: Superficial Courtship Mutantsmentioning
confidence: 99%