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Cited by 80Genetics and Neurodevelopmental DisordersAutism Spectrum Disorder ResearchNeurogenesis and neuroplasticity mechanisms

Dynamic gene and protein expression patterns of the autism‐associated met receptor tyrosine kinase in the developing mouse forebrain

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Judson, Matthew C., Bergman, Mica Y., Campbell, Daniel B., Eagleson, Kathie L., Levitt, Pat·2009·Journal of Comparative Neurology
DOI 10.1002/cne.21969PMC PMC2647986
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Abstract

The establishment of appropriate neural circuitry depends on the coordination of multiple developmental events across space and time. These events include proliferation, migration, differentiation, and survival—all of which can be mediated by hepatocyte growth factor (HGF) signaling through the Met receptor tyrosine kinase. We previously found a functional promoter variant of the MET gene to be associated with autism spectrum disorder, suggesting that forebrain circuits governing social and emotional function may be especially vulnerable to developmental disruptions in HGF/Met signaling. However, little is known about the spatiotemporal distribution of Met expression in the forebrain during the development of such circuits. To advance our understanding of the neurodevelopmental influences of Met activation, we employed complementary Western blotting, in situ hybridization, and immunohistochemistry to comprehensively map Met transcript and protein expression throughout perinatal and postnatal development of the mouse forebrain. Our studies reveal complex and dynamic spatiotemporal patterns of expression during this period. Spatially,Met transcript is localized primarily to specific populations of projection neurons within the neocortex and in structures of the limbic system, including the amygdala, hippocampus, and septum. Met protein appears to be principally located in axon tracts. Temporally, peak expression of transcript and protein occurs during the second postnatal week. This period is characterized by extensive neurite outgrowth and synaptogenesis, supporting a role for the receptor in these processes. Collectively, these data suggest that Met signaling may be necessary for the appropriate wiring of forebrain circuits, with particular relevance to the social and emotional dimensions of behavior. J. Comp. Neurol. 513:511–531, 2009. © 2009 Wiley‐Liss, Inc.

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  • MET is expressed throughout neocortex, hippocampus, cerebellum and brainstem, enriched in excitatory pre- and post-synaptic compartments.

    “MET is expressed throughout the neocortex, hippocampus180, cerebellum181 and brainstem182, where it is enriched in excitatory pre- and post-synaptic compartments183.”

    From Immune mediators in the brain and peripheral tissues in autism spectrum disorder (2015) · cites this paper as [181]

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Research works printed but not linked: 5

  1. Aggleton JP The amygdala: a functional analysis 2000 xiv 690 Oxford University Press Oxford, OX; New York
  2. Barrett S Beck JC Bernier R Bisson E Braun TA Casavant TL Childress D Folstein SE Garcia M Gardiner MB Gilman S Haines JL Hopkins K Landa R Meyer NH Mullane JA Nishimura DY Palmer P Piven J Purdy J Santangelo SL Searby C Sheffield V Singleton J Slager S An autosomal genomic screen for autism. Collaborative linkage study of autism American journal of medical genetics 1999 88 609 615 10581478
  3. Hockfield S Molecular probes of the nervous system; selected methods for antibody and nucleic acid probes 1993 xxii 679 Cold Spring Harbor Laboratory Press Plainview, NY
  4. IMGSAC A full genome screen for autism with evidence for linkage to a region on chromosome 7q International Molecular Genetic Study of Autism Consortium Hum Mol Genet 1998 7 571 578 9546821
  5. Risold PY Swanson LW Connections of the rat lateral septal complex Brain Res Brain Res Rev 1997 24 115 195 9385454

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Authors
Judson, M. C., Bergman, M. Y., Campbell, D. B., Eagleson, K. L., & Levitt, P.
Affiliations
Vanderbilt University Medical Center (US)
Corresponding author
Levitt, Pat
ORCID
Venue
Journal of Comparative Neurology
Publisher
Wiley
Published
2009-02-18
Volume
513
Issue
5
Pages
511-531
ISSN
  • 0021-9967 (ISSN-L)
  • 1096-9861
DOI
10.1002/cne.21969
PMC
PMC2647986
OpenAlex
W2150328639
Cited by
80
References
117
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 4 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 8 · 2016: 7 · 2015: 2 · 2014: 4 · 2013: 8 · 2012: 8
FWCI
5.00
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Comparative Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (MH67842, F30MH083474, MH083474, R01MH067842, R56MH067842)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD015052)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
MET receptor tyrosine kinase, autism spectrum disorder, forebrain development, spatiotemporal gene expression, projection neurons, neocortex, limbic system, amygdala, hippocampus, septum, axon tracts, neurite outgrowth, synaptogenesis, postnatal development
MeSH terms
Empty Spiracles Homeobox Proteins, Age Factors, Amygdala, Animals, Animals, Newborn, Autistic Disorder, Cell Differentiation, Embryo, Mammalian, Hippocampus, Immunohistochemistry, Limbic System, Mice, Inbred C57BL, Neurons, Transcription Factors, Blotting, Western, Signal Transduction, Polymerase Chain Reaction, Prosencephalon, In Situ Hybridization, Mice, Knockout, Homeodomain Proteins, Gene Expression Regulation, Developmental, Proto-Oncogene Proteins c-met, Receptor Protein-Tyrosine Kinases, Mice

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