The ability of stem cells to switch between quiescence and proliferation is crucial for tissue homeostasis and regeneration. Drosophila quiescent neural stem cells (NSCs) extend a primary cellular protrusion from the cell body prior to their reactivation. However, the structure and function of this protrusion are not well established. Here, we show that in the protrusion of quiescent NSCs, microtubules are predominantly acentrosomal and oriented plus-end-out toward the tip of the primary protrusion. We have identified Mini Spindles (Msps)/XMAP215 as a key microtubule regulator in quiescent NSCs that governs NSC reactivation via regulating acentrosomal microtubule growth and orientation. We show that quiescent NSCs form membrane contact with the neuropil and E-cadherin, a cell adhesion molecule, localizes to these NSC-neuropil junctions. Msps and a plus-end directed motor protein Kinesin-2 promote NSC cell cycle re-entry and target E-cadherin to NSC-neuropil contact during NSC reactivation. Together, this work establishes acentrosomal microtubule organization in the primary protrusion of quiescent NSCs and the Msps-Kinesin-2 pathway that governs NSC reactivation, in part, by targeting E-cad to NSC-neuropil contact sites.

中文翻译：

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Msps 控制着静止神经干细胞的中心体微管组装和再激活

干细胞在静止和增殖之间切换的能力对于组织稳态和再生至关重要。果蝇静止神经干细胞 (NSC) 在重新激活之前从细胞体中伸出初级细胞突起。然而，该突起的结构和功能尚未完全确定。在这里，我们表明在静止的 NSC 的突起中，微管主要是中心体，并且朝向初级突起的尖端定向。我们已将 Mini Spindles (Msps)/XMAP215 确定为静止 NSC 中的关键微管调节器，通过调节中心体微管生长和方向来控制 NSC 再激活。我们表明静止的 NSC 与神经纤维网和 E-钙粘蛋白（一种细胞粘附分子）形成膜接触，定位于这些 NSC-神经纤维网连接处。Msps 和正端定向运动蛋白 Kinesin-2 可促进 NSC 细胞周期重新进入，并在 NSC 重新激活期间将 E-钙粘蛋白靶向至 NSC-neuropil 接触。总之，这项工作通过将 E-cad 靶向 NSC-neuropil 接触位点，在静止的 NSC 的初级突起和控制 NSC 重新激活的 Msps-Kinesin-2 通路中建立了中心体微管组织。