Evidence map›Paper›PMID 10632594›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Novel mechanism of massive photoreceptor degeneration caused by mutations in the trp gene of Drosophila.

J Yoon, H C Ben-Ami, Y S Hong, S Park, L L Strong, J Bowman, C Geng, K Baek, B Minke, W L Pak

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

49 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  8. A Single Residue Mutation in the GαG3 (Bethesda, Md.) · 2018
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  9. Article
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  13. Article
  14. Article
  15. Article
  16. Progressive degeneration of dopaminergic neurons through TRP channel-induced cell death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  17. Article
  18. Compartmentalization and Ca2+ buffering are essential for prevention of light-induced retinal degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  19. Article
  20. Review
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

10 authors at 2 institutions in 2 countries.

J YoonInstitute of Genetic Engineering and Natural Sciences, Department of Genetic Engineering, KyungHee University, Yongin City, Kyungki-Do, 449-701 Korea.
H C Ben-Ami
Y S Hong
S Park
L L Strong
J Bowman
C Geng
K Baek
B Minke
W L Pak
Purdue University West Lafayette · USKyung Hee University · KR

Funding

MOLECULAR GENETIC DISSECTION OF PHOTORECEPTOR FUNCTIONR01EY000033 · NEI · PURDUE UNIVERSITY WEST LAFAYETTE · PI PAK, WILLIAM L · 1985 to 2008
$3.7M
GENETIC DISSECTION OF PHOTOTRANSDUCTIONR01EY003529 · NEI · HEBREW UNIVERSITY OF JERUSALEM · PI MINKE, BARUCH · 1985 to 2011
$1.8M
Molecular Genetic Dissection of Photoreceptor FunctionR56EY000033 · NEI · PURDUE UNIVERSITY · PI PAK, WILLIAM L · 2009 to 2009
$343k
MOLECULAR GENETIC DISSECTION OF PHOTORECEPTOR FUNCTIONR37EY000033 · NEI · PURDUE UNIVERSITY WEST LAFAYETTE · PI PAK, WILLIAM L · 1990 to 1999
–
NEI NIH HHS EY00033NEI NIH HHS EY03529NEI NIH HHS R01 EY000033NEI NIH HHS R01 EY003529NEI NIH HHS R37 EY000033NEI NIH HHS R56 EY000033
6 · The paper itself

Abstract

The Drosophila trp gene encodes a light-activated Ca(2+) channel subunit, which is a prototypical member of a novel class of channel proteins. Previously identified trp mutants are all recessive, loss-of-function mutants characterized by a transient receptor potential and the total or near-total loss of functional TRP protein. Although retinal degeneration does occur in these mutants, it is relatively mild and slow in onset. We report herein a new mutant, Trp(P365), that does not display the transient receptor potential phenotype and is characterized by a substantial level of the TRP protein and rapid, semi-dominant degeneration of photoreceptors. We show that, in spite of its unusual phenotypes, Trp(P365) is a trp allele because a Trp(P365) transgene induces the mutant phenotype in a wild-type background, and a wild-type trp transgene in a Trp(P365) background suppresses the mutant phenotype. Moreover, amino acid alterations that could cause the Trp(P365) phenotype are found in the transmembrane segment region of the mutant channel protein. Whole-cell recordings clarified the mechanism underlying the retinal degeneration by showing that the TRP channels of Trp(P365) are constitutively active. Although several genes, when mutated, have been shown to cause retinal degeneration in Drosophila, the underlying mechanism has not been identified for any of them. The present studies provide evidence for a specific mechanism for massive degeneration of photoreceptors in Drosophila. Insofar as some human homologs of TRP are highly expressed in the brain, a similar mechanism could be a major contributor to degenerative disorders of the brain.

Indexed as

Amino Acid SubstitutionChromosome MappingPoint MutationAmino Acid SequenceAnimalsCalcium ChannelsDrosophila melanogasterElectroretinographyGenes, InsectHumansMicroscopy, ConfocalMolecular Sequence DataNerve DegenerationPhenotypePhotoreceptor Cells, InvertebrateRetinaCalcium Channelstransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID10632594
PMCPMC6772429
OpenAlexW2170991485

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.