Evidence map›Paper›PMID 29207951›Full record

ArticleBMC neuroscience2017

Downstream mediators of Ten-m3 signalling in the developing visual pathway.

Kelly A Glendining, Sam C Liu, Marvin Nguyen, Nuwan Dharmaratne, Rajini Nagarajah, Miguel A Iglesias, Atomu Sawatari, Catherine A Leamey

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Kelly A GlendiningDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Sam C LiuDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Marvin NguyenDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Nuwan DharmaratneDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Rajini NagarajahDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Miguel A IglesiasDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Atomu SawatariDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia.
Catherine A LeameyDiscipline of Physiology, School of Medical Sciences and Bosch Institute, F13, University of Sydney, Sydney, NSW, 2006, Australia. cathy@physiol.usyd.edu.au.
University of Sydney · AU

Funding

National Health and Medical Research Council 632685University of Sydney Bridging Grant
6 · The paper itself

Abstract

backgroundThe formation of visuotopically-aligned projections in the brain is required for the generation of functional binocular circuits. The mechanisms which underlie this process are unknown. Ten-m3 is expressed in a broad high-ventral to low-dorsal gradient across the retina and in topographically-corresponding gradients in primary visual centres. Deletion of Ten-m3 causes profound disruption of binocular visual alignment and function. Surprisingly, one of the most apparent neuroanatomical changes-dramatic mismapping of ipsilateral, but not contralateral, retinal axons along the representation of the nasotemporal retinal axis-does not correlate well with Ten-m3's expression pattern, raising questions regarding mechanism. The aim of this study was to further our understanding of the molecular interactions which enable the formation of functional binocular visual circuits.

methodsAnterograde tracing, gene expression studies and protein pull-down experiments were performed. Statistical significance was tested using a Kolmogorov-Smirnov test, pairwise-fixed random reallocation tests and univariate ANOVAs.

resultsWe show that the ipsilateral retinal axons in Ten-m3 knockout mice are mismapped as a consequence of early axonal guidance defects. The aberrant invasion of the ventral-most region of the dorsal lateral geniculate nucleus by ipsilateral retinal axons in Ten-m3 knockouts suggested changes in the expression of other axonal guidance molecules, particularly members of the EphA-ephrinA family. We identified a consistent down-regulation of EphA7, but none of the other EphA-ephrinA genes tested, as well as an up-regulation of ipsilateral-determinants Zic2 and EphB1 in visual structures. We also found that Zic2 binds specifically to the intracellular domain of Ten-m3 in vitro.

conclusionOur findings suggest that Zic2, EphB1 and EphA7 molecules may work as effectors of Ten-m3 signalling, acting together to enable the wiring of functional binocular visual circuits.

Indexed as

AnimalsAxonsCell EnlargementFunctional LateralityGene Expression Regulation, DevelopmentalGeniculate BodiesIntracellular SpaceMembrane ProteinsMice, KnockoutNerve Tissue ProteinsReceptor, EphA7Receptor, EphB1Retinal Ganglion CellsSuperior ColliculiTranscription FactorsVision, Binocularepha7 receptor, mouseMembrane ProteinsNerve Tissue ProteinsReceptor, EphA7Receptor, EphB1Tenm3 protein, mouseTranscription FactorsZic2 protein, mouseBinocular visionContralateralEphA7IpsilateralNeural developmentRetinaRetinotopic mappingTeneurin/OdzZic2

Identifiers

PMID29207951
PMCPMC5718065
OpenAlexW2772489371

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.