miR‐31 mutants reveal continuous glial homeostasis in the adult Drosophila brain

The study of adult neural cell production has concentrated on neurogenesis. The mechanisms controlling adult gliogenesis are still poorly understood. Here, we provide evidence for a homeostatic process that maintains the population of glial cells in the Drosophila adult brain. Flies lacking microRNA...

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Veröffentlicht in:The EMBO journal 2017-05, Vol.36 (9), p.1215-1226
Hauptverfasser: Foo, Lynette Caizhen, Song, Shilin, Cohen, Stephen Michael
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Sprache:eng
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Zusammenfassung:The study of adult neural cell production has concentrated on neurogenesis. The mechanisms controlling adult gliogenesis are still poorly understood. Here, we provide evidence for a homeostatic process that maintains the population of glial cells in the Drosophila adult brain. Flies lacking microRNA miR‐31a start adult life with a normal complement of glia, but transiently lose glia due to apoptosis. miR‐31a expression identifies a subset of predominantly gliogenic adult neural progenitor cells. Failure to limit expression of the predicted E3 ubiquitin ligase, Rchy1, in these cells results in glial loss. After an initial decline in young adults, glial numbers recovered due to compensatory overproduction of new glia by adult progenitor cells, indicating an unexpected plasticity of the Drosophila nervous system. Experimentally induced ablation of glia was also followed by recovery of glia over time. These studies provide evidence for a homeostatic mechanism that maintains the number of glia in the adult fly brain. Synopsis The adult fly brain shows continued glial turnover mediated by a novel miR‐31a ‐expressing gliogenic progenitor pool. Glia turnover in substantial number in young adult brains is replaced by a homeostatic mechanism miR‐31a expression defines a predominantly gliogenic adult progenitor cell Overexpression of Rchy1 in progenitors in miR‐31a mutants impairs production of new glia Graphical Abstract The adult fly brain shows continued glial turnover mediated by a novel miR‐31a ‐expressing gliogenic progenitor pool.
ISSN:0261-4189
1460-2075
DOI:10.15252/embj.201695861