Lynette Caizhen Foo* , Shilin Song† & Stephen Michael Cohen
* Corresponding author. Tel: +65 6586 9721; E-mail: firstname.lastname@example.org
**Corresponding author. Tel: +45 3532 7326; E-mail: email@example.com
† Present address: Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark
Published online in The EMBO Journal on 20 March 2017.
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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 homeo- static 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 predomi- nantly 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 stud- ies provide evidence for a homeostatic mechanism that maintains the number of glia in the adult fly brain.
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