Evidence map›Paper›PMID 23077055›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Compartmentalization and Ca2+ buffering are essential for prevention of light-induced retinal degeneration.

Shirley Weiss, Elkana Kohn, Daniela Dadon, Ben Katz, Maximilian Peters, Mario Lebendiker, Mickey Kosloff, Nansi Jo Colley, Baruch Minke

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Loss of calcium-binding proteinbioRxiv : the preprint server for biology · 2026
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  6. Knockdown of Dehydrodolichyl Diphosphate Synthase in theFrontiers in molecular neuroscience · 2021
    Article
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  10. Ectopic Expression of Mouse Melanopsin inThe Journal of biological chemistry · 2017
    Article
  11. Article
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  14. Article
  15. Separate Ca2+ sources are buffered by distinct Ca2+ handling systems in aplysia neuroendocrine cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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

9 authors at 3 institutions in 2 countries.

Shirley WeissDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada (IMRIC) and the Edmond and Lily Safra Center for Brain Sciences (ELSC), Faculty of Medicine, the Hebrew University, Jerusalem 91120, Israel.
Elkana Kohn
Daniela Dadon
Ben Katz
Maximilian Peters
Mario Lebendiker
Mickey Kosloff
Nansi Jo Colley
Baruch Minke
Hebrew University of Jerusalem · ILUniversity of Haifa · ILUniversity of Wisconsin–Madison · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
MOLECULAR STUDIES OF RETINAL DEGENERATION IN DROSOPHILAR01EY008768 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI COLLEY, NANSI J. · 1995 to 2016
$5.3M
GENETIC DISSECTION OF PHOTOTRANSDUCTIONR01EY003529 · NEI · HEBREW UNIVERSITY OF JERUSALEM · PI MINKE, BARUCH · 1985 to 2011
$1.8M
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY003529NEI NIH HHS R01 EY008768NEI NIH HHS R01 EY03529
6 · The paper itself

Abstract

Fly photoreceptors are polarized cells, each of which has an extended interface between its cell body and the light-signaling compartment, the rhabdomere. Upon intense illumination, rhabdomeric calcium concentration reaches millimolar levels that would be toxic if Ca(2+) diffusion between the rhabdomere and cell body was not robustly attenuated. Yet, it is not clear how such effective attenuation is obtained. Here we show that Ca(2+) homeostasis in the photoreceptor cell relies on the protein calphotin. This unique protein functions as an immobile Ca(2+) buffer localized along the base of the rhabdomere, separating the signaling compartment from the cell body. Generation and analyses of transgenic Drosophila strains, in which calphotin-expression levels were reduced in a graded manner, showed that moderately reduced calphotin expression impaired Ca(2+) homeostasis while calphotin elimination resulted in severe light-dependent photoreceptor degeneration. Electron microscopy, electrophysiology, and optical methods revealed that the degeneration was rescued by prevention of Ca(2+) overload via overexpression of CalX, the Na(+)-Ca(2+) exchanger. In addition, Ca(2+)-imaging experiments showed that reduced calphotin levels resulted in abnormally fast kinetics of Ca(2+) elevation in photoreceptor cells. Together, the data suggest that calphotin functions as a Ca(2+) buffer; a possibility that we directly demonstrate by expressing calphotin in a heterologous expression system. We propose that calphotin-mediated compartmentalization and Ca(2+) buffering constitute an effective strategy to protect cells from Ca(2+) overload and light-induced degeneration.

Indexed as

AnimalsAnimals, Genetically ModifiedBuffersCalciumCalcium-Binding ProteinsCell CompartmentationDark AdaptationDrosophila melanogasterDrosophila ProteinsHEK293 CellsHumansHydrogen-Ion ConcentrationLightPhotoreceptor Cells, InvertebrateRetinal DegenerationBuffersCalciumCalcium-Binding ProteinsCpn protein, DrosophilaDrosophila Proteins

Identifiers

PMID23077055
PMCPMC3492704
OpenAlexW2020392635

What OpenQuestion holds

Textmetadata
LicenceTDM
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.