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Molecular basis of an inherited retinal defect in Drosophila.
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1985
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GeneticsGenomic MechanismMolecular GeneticsOptogeneticsNormal Visual TransductionTrp GeneRetinaMolecular AdaptationOphthalmologyDevelopmental GeneticsInherited Retinal DefectReceptor PotentialGene ExpressionBiologyPhotoreceptor CellDevelopmental BiologyNatural SciencesGenetic MechanismMedicineRetinal Biology
Fruitflies carrying the autosomal recessive mutation transient receptor potential (trp) are blind in bright light because the receptor potential of such a mutant decays almost completely during an intense stimulus. The trp gene has been localized and a set of partially overlapping genomic clones that include the trp gene has been isolated. The stretch of DNA represented by these genomic clones is found to contain genes that encode for four RNA species. Two of these RNA species are missing in the mutant. This observation is consistent with the notion that the mutation alters the DNA sequence in a region containing signals necessary for the expression of the gene. Accordingly, the molecular basis of the mutant phenotype may be due to the lack of a protein(s) that is/are important for normal visual transduction.