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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. SYNOPSIS: In the primary protrusion of quiescent neural stem cells (NSCs), microtubules are predominantly acentrosomal and oriented plus‐end‐out. Msps/XMAP215 and Kinesin‐2 promote NSC cell cycle re‐entry and target E‐cadherin to NSC‐neuropil contact during NSC reactivation. In the primary protrusion of quiescent NSCs, microtubules are predominantly acentrosomal and oriented plus‐end‐out.Mini Spindles (Msps)/XMAP215 is a key regulator of acentrosomal microtubule growth and orientation in the primary protrusion of quiescent NSCs.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. [ABSTRACT FROM AUTHOR]

MOR1, the Arabidopsis thaliana homologue of the Xenopus microtubule-associated protein MAP215, is required for spatial organization of the acentrosomal microtubule arrays of plant cells. To determine how loss of MOR1 function affects microtubule dynamics, we compared various parameters of microtubule dynamics in the temperature-sensitive mor1-1 mutant at its permissive and restrictive temperatures, 21°C and 31°C, respectively. Dynamic events were tracked in live cells expressing either GFP-tagged β-tubulin or the plus end tracking EB1. Microtubule growth and shrinkage velocities were both dramatically reduced in mor1-1 at 31°C and the incidence and duration of pause events increased. Interestingly, the association of EB1 with microtubule plus ends was reduced in mor1-1 whereas side wall binding increased, suggesting that MOR1 influences the association of EB1 with microtubules either by modulating microtubule plus end structure or by interacting with EB1. Although mor1-1 microtubules grew and shrank more slowly than wild-type microtubules at 21°C, the incidence of pause was not altered, suggesting that pause events, which occur more frequently at 31°C, have a major detrimental role in the spatial organization of cortical microtubules. Extensive increases in microtubule dynamics in wild-type cells when shifted from 21°C to 31°C underline the importance of careful temperature control in live cell imaging. [ABSTRACT FROM AUTHOR]