Evidence map›Paper›PMID 1551579›Full record

ArticleGenetics1992

Nonsense suppression of the major rhodopsin gene of Drosophila.

T Washburn, J E O'Tousa

Abstract read
In one paragraph

Article in Genetics, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  10. Limited role of developmental programmed cell death pathways in Drosophila norpA retinal degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
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  14. Invertebrate synapsins: a single gene codes for several isoforms in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

T WashburnDepartment of Biological Sciences, University of Notre Dame, Indiana 46556.
J E O'Tousa
University of Notre Dame · US

Funding

NEI NIH HHS EY06808
6 · The paper itself

Abstract

We placed UAA, UAG and UGA nonsense mutations at two leucine codons, Leu205 and Leu309, in Drosophila's major rhodopsin gene, ninaE, by site-directed mutagenesis, and then created the corresponding mutants by P element-mediated transformation of a ninaE deficiency strain. In the absence of a genetic suppressor, flies harboring any of the nonsense mutations at the 309 site, but not the 205 site, show increased rhodopsin activity. Additionally, all flies with nonsense mutations at either site have better rhabdomere structure than does the ninaE deficiency strain. Construction and analysis of a 3'-deletion mutant of ninaE indicates that translational readthrough accounts for the extra photoreceptor activity of the ninaE309 alleles and that truncated opsins are responsible for the improved rhabdomere structure. The presence of leucine-inserting tRNA nonsense suppressors DtLa Su+ and DtLb Su+ in the mutant strains produced a small increase (less than 0.04%) in functional rhodopsin. The opal (UGA) suppressor derived from the DtLa tRNA gene is more efficient than the amber (UAG) or opal suppressor derived from the DtLb gene, and both DtLa and DtLb derived suppressors are more efficient at site 205 than 309.

Indexed as

Suppression, GeneticAllelesAmino Acid SequenceAnimalsBase SequenceDNADrosophilaElectrophysiologyMicroscopy, ElectronMolecular Sequence DataMutagenesis, Site-DirectedPhenotypePhotoreceptor CellsProtein ConformationRhodopsinDNARhodopsin

Identifiers

PMID1551579
PMCPMC1204875
OpenAlexW2263048600

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.