Abstract
Brain stem cells stop dividing in late Drosophila embryos and begin dividing again in early larvae after feeding induces reactivation. Quiescent neural stem cells (qNSCs) display an unusual cytoplasmic protrusion that is no longer present in reactivated NSCs. The protrusions join the qNSCs to the neuropil, brain regions that are thought to maintain NSCs in an undifferentiated state, but the function of the protrusions is not known. Here we show that qNSC protrusions contain clustered mitochondria that are likely maintained in position by slow forward-and-backward microtubule growth. Larvae treated with a microtubule-stabilizing drug show bundled microtubules and enhanced mitochondrial clustering in NSCs, together with reduced qNSC reactivation. We further show that intestinal stem cells contain mitochondria-enriched protrusions. The qNSC and intestinal stem-cell protrusions differ from previously reported cytoplasmic extensions by forming stem-cell-to-niche mitochondrial bridges that could potentially both silence genes and sense signals from the stem cell niche.
Highlights
Brain stem cells stop dividing in late Drosophila embryos and begin dividing again in early larvae after feeding induces reactivation
We further show that other insulinsensitive stem cells—Drosophila midgut intestinal stem cells (ISCs)—contain mitochondrial-rich protrusions
The Quiescent neural stem cells (qNSCs) and ISC cytoplasmic protrusions both form stem-cellto-niche bridges containing mitochondria along their length, despite their morphological differences—the qNSC protrusions are thin and can extend up to ~45 μm from the cell body to the neuropil, whereas the lamellipodia-like protrusions associated with putative ISCs extend only up to ~8 μm from the nucleus to the cell membrane
Summary
Brain stem cells stop dividing in late Drosophila embryos and begin dividing again in early larvae after feeding induces reactivation. QNSCs in tVNCs, as well as BLs, showed mitochondria distributed along protrusions and clustered in cell bodies by mito-RFP fluorescence in fixed or live larval brains (Fig. 2d, e and Supplementary Fig. 2).
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