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. 2016 May 9;213(3):315–328. doi: 10.1083/jcb.201510117

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© 2016 Kern et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 8. — Model for Astrin/SKAP complex plus-end tracking activity in promoting proper spindle positioning. (A) Schematic for a model explaining spindle behavior in control cells (left) and SKAP ΔEB mutant cells (right). In wild-type cells, the Astrin/SKAP complex localizes to microtubule plus ends along with Clasp1 and other factors. In these cells, astral microtubules make transient, end-on contacts with the cell cortex and cortical dynein to generate short bursts of force to position the spindle. In SKAP ΔEB cells, the Astrin/SKAP complex is eliminated from microtubule plus ends. In this condition, metaphase astral microtubules make longer-lasting, lateral contacts with cortex and cortical dynein. These persistent connections lead to significant spindle position shifts from stochastic force imbalances and sustained pulling force from cortical dynein. (B) Hypothetical docking model for astral microtubules on cortex. We propose that the Astrin/SKAP complex, along with Clasp1 and other unknown proteins, mediates an engagement between microtubule plus ends and cortical dynein. This docking may be necessary for proper regulation of microtubule dynamics and dynein force production.