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Defective cortex glia plasma membrane structure underlies light-induced epilepsy in cpes mutants

  1. Author:
    Kunduri, Govind
    Turner-Evans, Daniel
    Konya, Yutaka
    Izumi, Yoshihiro [ORCID]
    Nagashima, Kunio
    Lockett, Stephen
    Holthuis, Joost
    Bamba, Takeshi
    Acharya, Usha
    Acharya, Jairaj [ORCID]

  2. Author Address

    Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD 21702., Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147., Department of Metabolomics, Kyushu University, Fukuoka 812-8582, Japan., Electron Microscopy Laboratory, National Cancer Institute, Frederick, MD 21702., Optical Microscopy and Analysis Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD 21702., Molecular Cell Biology Division, University of Osnabr 252;ck, 49074 Osnabr 252;ck, Germany., Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605., Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD 21702; acharyaj@mail.nih.gov.,
    1. Year: 2018
    2. Date: Sep 18
    3. Epub Date: 2018 09 05
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 115
    2. 38
    3. Pages: E8919-E8928
  4. Type of Article: Article
  5. ISSN: 0027-8424
  1. Abstract:

    Seizures induced by visual stimulation (photosensitive epilepsy; PSE) represent a common type of epilepsy in humans, but the molecular mechanisms and genetic drivers underlying PSE remain unknown, and no good genetic animal models have been identified as yet. Here, we show an animal model of PSE, in Drosophila, owing to defective cortex glia. The cortex glial membranes are severely compromised in ceramide phosphoethanolamine synthase (cpes)-null mutants and fail to encapsulate the neuronal cell bodies in the Drosophila neuronal cortex. Expression of human sphingomyelin synthase 1, which synthesizes the closely related ceramide phosphocholine (sphingomyelin), rescues the cortex glial abnormalities and PSE, underscoring the evolutionarily conserved role of these lipids in glial membranes. Further, we show the compromise in plasma membrane structure that underlies the glial cell membrane collapse in cpes mutants and leads to the PSE phenotype. Copyright © 2018 the Author(s). Published by PNAS.

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External Sources

  1. View Full Text
  2. DOI: 10.1073/pnas.1808463115
  3. PMID: 30185559
  4. View record in Web of Science®
  5. WOS: 000447224900012
  6. PII : 1808463115

Library Notes

  1. Fiscal Year: FY2017-2018
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