Evidence map›Paper›PMID 21328570›Full record

ArticleAutism research : official journal of the International Society for Autism Research2011

The autism risk genes MET and PLAUR differentially impact cortical development.

Kathie L Eagleson, Daniel B Campbell, Barbara L Thompson, Mica Y Bergman, Pat Levitt

Open access · bronzeAbstract read
In one paragraph

Article in Autism research : official journal of the International Society for Autism Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

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  10. The Gain-of-Function Integrin β3 Pro33 Variant Alters the Serotonin System in the Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Kathie L EaglesonZilkha Neurogenetic Institute, Keck School of Medicine at USC, Los Angeles, California 90033, USA. keagleso@usc.edu
Daniel B Campbell
Barbara L Thompson
Mica Y Bergman
Pat Levitt
Keck Hospital of USC · USVanderbilt University Medical Center · US

Funding

Function &Structure Adaptation in Forebrain DevelopmentR01MH067842 · NIMH · VANDERBILT UNIVERSITY · PI LEVITT, PAT · 2002 to 2023
$10.8M
Regulation of MET Expression in Autism Disorder and Forebrain OntogenyF30MH083474 · NIMH · VANDERBILT UNIVERSITY · PI BERGMAN, MICA Y. · 2007 to 2009
$77k
NIMH NIH HHS F30 MH083474NIMH NIH HHS R01 MH067842
6 · The paper itself

Abstract

Candidate risk genes for autism spectrum disorder (ASD) have been identified, but the challenge of determining their contribution to pathogenesis remains. We previously identified two ASD risk genes encoding the receptor tyrosine kinase MET and the urokinase plasminogen activator receptor (PLAUR), which is thought to modulate availability of the MET ligand. We also reported a role for Met signaling in cortical interneuron development in vitro and a reduction of these neurons in uPAR (mouse ortholog of PLAUR) null mice, suggesting that disruption of either gene impacts cortical development similarly. Here, we modify this conclusion, reporting that interneuron numbers are unchanged in the neocortex of Met(fx/fx) / Dlx5/6(cre) mice, in which Met is ablated from cells arising from the ventral telencephalon (VTel). Consistent with this, Met transcript is not detected in the VTel during interneuron genesis and migration; furthermore, during the postnatal period of interneuron maturation, Met is co-expressed in glutamatergic projection neurons, but not interneurons. Low levels of Met protein are expressed in the VTel at E12.5 and E14.5, likely reflecting the arrival of Met containing corticofugal axons. Met expression, however, is induced in E12.5 VTel cells after 2 days in vitro, perhaps underlying discrepancies between observations in vitro and in Met(fx/fx) / Dlx5/6(cre) mice. We suggest that, in vivo, Met impacts the development of cortical projection neurons, whereas uPAR influences interneuron maturation. An altered balance between excitation and inhibition has been postulated as a biological mechanism for ASD; this imbalance could arise from different risk genes differentially affecting either or both elements.

Indexed as

AllelesAnimalsCell CountCell MovementCerebral CortexChildChild Development Disorders, PervasiveGene ExpressionGenetic Association StudiesHippocampusHumansIn Situ HybridizationInterneuronsIn Vitro TechniquesMalformations of Cortical DevelopmentMicePlaur protein, mouseProto-Oncogene Proteins c-metReceptors, Urokinase Plasminogen Activator

Identifiers

PMID21328570
PMCPMC3644181
OpenAlexW1989447435

What OpenQuestion holds

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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.