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Citation
Aw, S.S., Lim, I.K.H., Tang, M.X.M., Cohen, S.M. (2017). A Glio-Protective Role of mir-263a by Tuning Sensitivity to Glutamate.  Cell Rep. 19(9): 1783--1793.
FlyBase ID
FBrf0235674
Publication Type
Research paper
Abstract

Glutamate is a ubiquitous neurotransmitter, mediating information flow between neurons. Defects in the regulation of glutamatergic transmission can result in glutamate toxicity, which is associated with neurodegeneration. Interestingly, glutamate receptors are expressed in glia, but little is known about their function, and the effects of their misregulation, in these non-neuronal cells. Here, we report a glio-protective role for Drosophila mir-263a mediated by its regulation of glutamate receptor levels in glia. mir-263a mutants exhibit a pronounced movement defect due to aberrant overexpression of CG5621/Grik, Nmdar1, and Nmdar2. mir-263a mutants exhibit excitotoxic death of a subset of astrocyte-like and ensheathing glia in the CNS. Glial-specific normalization of glutamate receptor levels restores cell numbers and suppresses the movement defect. Therefore, microRNA-mediated regulation of glutamate receptor levels protects glia from excitotoxicity, ensuring CNS health. Chronic low-level glutamate receptor overexpression due to mutations affecting microRNA (miRNA) regulation might contribute to glial dysfunction and CNS impairment.

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Obtained with permission from Cell Press.
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    Language of Publication
    English
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    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Cell Rep.
    Title
    Cell reports
    ISBN/ISSN
    2211-1247
    Data From Reference
    Aberrations (5)
    Alleles (116)
    Genes (99)
    Human Disease Models (1)
    Natural transposons (2)
    Insertions (10)
    Experimental Tools (2)
    Transgenic Constructs (23)
    Transcripts (5)