Evidence map›Paper›PMID 21897116›Full record

ReviewFly

Molecular genetics of retinal degeneration: A Drosophila perspective.

Bih-Hwa Shieh

Open access · greenAbstract readReview
In one paragraph

Review in Fly. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  8. Application of Fluorescent Proteins for Functional Dissection of theInternational journal of molecular sciences · 2021
    Review
  9. Article
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  11. Drosophila Rhodopsin 7 can partially replace the structural role of Rhodopsin 1, but not its physiological function.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017
    Article
  12. Frontiers in neuroscience · 2017
    Article
  13. Article
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  16. Role of rhodopsin and arrestin phosphorylation in retinal degeneration of Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. Article
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

1 author at 1 institution in 1 country.

Bih-Hwa ShiehDepartment of Pharmacology, Center for Molecular Neuroscience and Vision Research Center, Vanderbilt University, Nashville, TN USA. bih-hwa.shieh@vanderbilt.edu
Vanderbilt University · US

Funding

Regulation of Drosophila arrestins in light adaptationR01EY019519 · NEI · VANDERBILT UNIVERSITY · PI SHIEH, BIH-HWA · 2009 to 2012
$1.5M
NEI NIH HHS R01 EY019519
6 · The paper itself

Abstract

Inherited retinal degeneration in Drosophila has been explored for insights into similar processes in humans. Based on the mechanisms, I divide these mutations in Drosophila into three classes. The first consists of genes that control the specialization of photoreceptor cells including the morphogenesis of visual organelles  (rhabdomeres) that house the visual signaling proteins. The second class contains genes that regulate the activity or level of the major rhodopsin, Rh1, which is the light sensor and also provides a structural role for the maintenance of rhabdomeres. Some mutations in Rh1 (NinaE) are dominant due to constitutive activity or folding defects, like autosomal dominant retinitis pigmentosa (ADRP) in humans. The third class consists of genes that control the Ca ( 2+) influx directly or indirectly by promoting the turnover of the second messenger and regeneration of PIP 2, or mediate the Ca ( 2+) -dependent regulation of the visual response. These gene products are critical for the increase in cytosolic Ca ( 2+ ) following light stimulation to initiate negative regulatory events. Here I will focus on the signaling mechanisms underlying the degeneration in norpA, and in ADRP-type NinaE mutants that produce misfolded Rh1. Accumulation of misfolded Rh1 in the ER triggers the unfolded protein response (UPR), while endosomal accumulation of activated Rh1 may initiate autophagy in norpA. Both autophagy and the UPR are beneficial for relieving defective endosomal trafficking and the ER stress, respectively. However, when photoreceptors fail to cope with the persistence of these stresses, a cell death program is activated leading to retinal degeneration.

Indexed as

AnimalsAutophagyCalciumDisease Models, AnimalDrosophilaDrosophila ProteinsHumansModels, BiologicalPhospholipase C betaPhotoreceptor Cells, InvertebrateProtein FoldingRetinal DegenerationRhodopsinSignal TransductionCalciumDrosophila ProteinsninaE protein, DrosophilaNorpA protein, DrosophilaPhospholipase C betaRhodopsin

Identifiers

PMID21897116
PMCPMC3266078
OpenAlexW2149492940

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.