Evidence map›Paper›PMID 18378571›Full record

ArticleInvestigative ophthalmology & visual science2008

Involvement of OA1, an intracellular GPCR, and G alpha i3, its binding protein, in melanosomal biogenesis and optic pathway formation.

Alejandra Young, Elisabeth B Powelson, Irene E Whitney, Mary A Raven, Steven Nusinowitz, Meisheng Jiang, Lutz Birnbaumer, Benjamin E Reese, Debora B Farber

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  18. Signaling pathways in melanosome biogenesis and pathology.The international journal of biochemistry & cell biology · 2010
    Review
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  20. 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 2 institutions in 1 country.

Alejandra YoungJules Stein Eye Institute, University of California, Los Angeles School of Medicine, Los Angeles, California 90095, USA.
Elisabeth B Powelson
Irene E Whitney
Mary A Raven
Steven Nusinowitz
Meisheng Jiang
Lutz Birnbaumer
Benjamin E Reese
Debora B Farber
University of California, Santa Barbara · USUniversity of California, Los Angeles · US

Funding

Transmembrane Signaling MechanismsZIGES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2009 to 2010
$5.3M
Transgenic/Molecular Approaches for Ocular AlbinismR01EY015141 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FARBER, DEBORA B · 2003 to 2006
$1.1M
Intramural NIH HHSNEI NIH HHS EY015141NEI NIH HHS R01 EY015141
6 · The paper itself

Abstract

purposeOcular albinism type 1 (OA1) is characterized by abnormalities in retinal pigment epithelium (RPE) melanosomes and misrouting of optic axons. The OA1 gene encodes a G-protein-coupled receptor (GPCR) that coimmunoprecipitates with the G alpha i-subunit of heterotrimeric G-proteins from human melanocyte extracts. This study was undertaken to test whether one of the G alpha i proteins, G alpha i3, signals in the same pathway as OA1 to regulate melanosome biogenesis and axonal growth through the optic chiasm.

methodsAdult G alpha i3(-/-) and Oa1(-/-) mice were compared with their respective control mice (129Sv and B6/NCrl) to study the effects of the loss of G alpha i3 or Oa1 function. Light and electron microscopy were used to analyze the morphology of the retina and the size and density of RPE melanosomes, electroretinograms to study retinal function, and retrograde labeling to investigate the size of the uncrossed optic pathway.

resultsAlthough G alpha i3(-/-) and Oa1(-/-) photoreceptors were comparable to those of the corresponding control retinas, the density of their RPE melanosomes was significantly lower than in control RPEs. In addition, the RPE cells of G alpha i3(-/-) and Oa1(-/-) mice showed abnormal melanosomes that were far larger than the largest 129Sv and B6/NCrl melanosomes, respectively. Although G alpha i3(-/-) and Oa1(-/-) mice had normal results on electroretinography, retrograde labeling showed a significant reduction from control in the size of their ipsilateral retinofugal projections.

conclusionsThese results indicate that G alpha i3, like Oa1, plays an important role in melanosome biogenesis. Furthermore, they suggest a common Oa1-G alpha i3 signaling pathway that ultimately affects axonal growth through the optic chiasm.

Indexed as

AnimalsAxonsCarrier ProteinsCell CountElectroretinographyEye ProteinsGTP-Binding Protein alpha Subunits, Gi-GoIntracellular MembranesMelanosomesMembrane GlycoproteinsMiceMice, KnockoutMicroscopy, ElectronOptic ChiasmPhenotypePigment Epithelium of EyeCarrier ProteinsEye ProteinsGnai3 protein, mouseGpr143 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoMembrane GlycoproteinsReceptors, G-Protein-Coupled

Identifiers

PMID18378571
PMCPMC2881626
OpenAlexW2036454380

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Registered trials

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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.