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. 2022 Jan 28;10:787294. doi: 10.3389/fcell.2022.787294

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Copyright © 2022 Barbosa, Sunkel and Conde.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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AURORA B-dependent regulation of KT-MT attachment stability. (A), B) Spatial positioning models for AURORA B function based on a (A) diffusible phosphorylation gradient or (B) physical distance between the kinase and substrates. Both models predict that the increase in inter-KT tension as a result of correct amphitelic KT-MT attachments pulls KT substrates away from the zone of influence of active AURORA B. (C) Model for the regulation of KT-localized AURORA B function. In this model, the gradual increase in KT-MT attachment stability evicts AURORA B from KTs which, in turn, further stabilizes KT-MT interactions. Dephosphorylation of AURORA B substrates like NDC80, KNL1 and the SKAc contributes to stabilize load-bearing end-on attachments. Interestingly, the SKAc recruits PP1 to KTs, but it remains elusive whether such PP1 pool contributes to the stabilization of KT-MT interactions (“?”).