Abstract

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.

Highlights

  • Glia outnumber neurons in the human brain and are critical for providing passive trophic support for neurons

  • Discussion miR-31a acts in adult glial progenitors to support glial cell survival

  • Despite the critical role that glia play in the proper functioning of neurons, study of adult neural cell production has focused mainly on neurons

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Summary

Introduction

Glia outnumber neurons in the human brain and are critical for providing passive trophic support for neurons. Glia serve important active roles in sculpting the nervous system and modulating synaptic connectivity (Allen et al, 2012; Schafer et al, 2012; Chung et al, 2013). Glia play important roles during development and to support normal functioning of the adult brain. Despite recent advances in understanding the functions of glia, little is known about the mechanisms underlying their development or their maintenance in the adult. Recent work has shown that Drosophila melanogaster glia perform functions very similar to those in mammals.

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