Sherry Shiying Aw1*, Isaac Kok Hwee Lim1, Melissa Xue Mei Tang1,
and Stephen Michael Cohen1,2*
1 Institute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology and Research), 61 Biopolis Drive, 138673, Singapore
2 Present address
Department of Cellular and Molecular Medicine
University of Copenhagen Blegdamsvej 3, Copenhagen 2200N, Denmark
Published in Cell Reports on May 30, 2017.
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 miRNA regulation might contribute to glial dysfunction and CNS impairment.
Drosophila mir-263a serves a glio-protective role mediated by its regulation of glutamate receptor levels in astrocyte-like and ensheathing glia.
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