Imp and Syp RNA-binding proteins govern decommissioning ofDrosophilaneural stem cells
Author(s) -
Ching-Po Yang,
Tamsin J. Samuels,
YaLing Huang,
Yang Lu,
David IshHorowicz,
Ilan Davis,
Tzumin Lee
Publication year - 2017
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.149500
Subject(s) - biology , mushroom bodies , microbiology and biotechnology , neuroblast , ecdysone receptor , neural stem cell , cell cycle , nuclear decommissioning , ecdysone , stem cell , drosophila melanogaster , genetics , transcription factor , nuclear receptor , cell , neurogenesis , gene , chemistry , nuclear chemistry
The termination of the proliferation of Drosophila neural stem cells, also known as neuroblasts (NBs), requires a 'decommissioning' phase that is controlled in a lineage-specific manner. Most NBs, with the exception of those of the mushroom body (MB), are decommissioned by the ecdysone receptor and mediator complex, causing them to shrink during metamorphosis, followed by nuclear accumulation of Prospero and cell cycle exit. Here, we demonstrate that the levels of Imp and Syp RNA-binding proteins regulate NB decommissioning. Descending Imp and ascending Syp expression have been shown to regulate neuronal temporal fate. We show that Imp levels decline slower in the MB than in other central brain NBs. MB NBs continue to express Imp into pupation, and the presence of Imp prevents decommissioning partly by inhibiting the mediator complex. Late-larval induction of transgenic Imp prevents many non-MB NBs from decommissioning in early pupae. Moreover, the presence of abundant Syp in aged NBs permits Prospero accumulation that, in turn, promotes cell cycle exit. Together, our results reveal that progeny temporal fate and progenitor decommissioning are co-regulated in protracted neuronal lineages.
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