ArticleThe Journal of general physiology1986
Electrophysiological study of Drosophila rhodopsin mutants.
Article in The Journal of general physiology, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 86 citations in OpenAlex.
- Progressive mitochondrial dysfunction impairs visual signal transduction and induces retinal degeneration inFrontiers in insect science · 2025Article
- Temperature and Sweet Taste Integration in Drosophila.Current biology : CB · 2020Article
- Sequence, Structure, and Expression of Opsins in the Monochromatic Stomatopod Squilla empusa.Integrative and comparative biology · 2018Article
- Cellular evidence for efference copy in Drosophila visuomotor processing.Nature neuroscience · 2015Article
- Loss of Na(+)/K(+)-ATPase in Drosophila photoreceptors leads to blindness and age-dependent neurodegeneration.Experimental neurology · 2014Article
- PDA (prolonged depolarizing afterpotential)-defective mutants: the story of nina's and ina's--pinta and santa maria, too.Journal of neurogenetics · 2012Review
- A Drosophila metallophosphoesterase mediates deglycosylation of rhodopsin.The EMBO journal · 2011Article
- Article
- Light-induced translocation of Drosophila visual Arrestin2 depends on Rac2.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- DAG lipase activity is necessary for TRP channel regulation in Drosophila photoreceptors.Neuron · 2008Article
- Presynaptic calcium channel localization and calcium-dependent synaptic vesicle exocytosis regulated by the Fuseless protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Prolonged G(q) activity triggers fly rhodopsin endocytosis and degradation, and reduces photoreceptor sensitivity.The EMBO journal · 2007Article
- Phototransduction and retinal degeneration in Drosophila.Pflugers Archiv : European journal of physiology · 2007Review
- Dissection of the pathway required for generation of vitamin A and for Drosophila phototransduction.The Journal of cell biology · 2007Article
- Calnexin is essential for rhodopsin maturation, Ca2+ regulation, and photoreceptor cell survival.Neuron · 2006Article
- Retrograde signaling from the brain to the retina modulates the termination of the light response in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Novel dominant rhodopsin mutation triggers two mechanisms of retinal degeneration and photoreceptor desensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Light adaptation in Drosophila photoreceptors: I. Response dynamics and signaling efficiency at 25 degrees C.The Journal of general physiology · 2001Article
- Phenotypes of trpl mutants and interactions between the transient receptor potential (TRP) and TRP-like channels in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- INAF, a protein required for transient receptor potential Ca(2+) channel function.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Electrophysiological investigations were carried out on several independently isolated mutants of the ninaE gene, which encodes opsin in R1-6 photoreceptors, and a mutant of the ninaD gene, which is probably important in the formation of the rhodopsin chromophore. In these mutants, the rhodopsin content in R1-6 photoreceptors is reduced by 10(2)-10(6)-fold. Light-induced bumps recorded from even the most severely affected mutants are physiologically normal. Moreover, a detailed noise analysis shows that photoreceptor responses of both a ninaE mutant and a ninaD mutant follow the adapting bump model. Since any extensive rhodopsin-rhodopsin interactions are not likely in these mutants, the above results suggest that such interactions are not needed for the generation and adaptation of light-induced bumps. Mutant bumps are strikingly larger in amplitude than wild-type bumps. This difference is observed both in ninaD and ninaE mutants, which suggests that it is due to severe depletion of rhodopsin content, rather than to any specific alterations in the opsin protein. Lowering or buffering the intracellular calcium concentration by EGTA injection mimics the effects of the mutations on the bump amplitude, but, unlike the mutations, it also affects the latency and kinetics of light responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.