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 |
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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. |
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ISSN: | 0261-4189 1460-2075 |
DOI: | 10.15252/embj.201695861 |