Clathrin's adaptor interaction sites are repurposed to stabilize microtubules during mitosis

Rondelet A, Lin YC, Singh D, Porfetye AT, Thakur HC, Hecker A, Brinkert P, Schmidt N, Bendre S, Müller F, Mazul L, Widlund PO, Bange T, Hiller M, Vetter IR, Bird AW (2020). J Cell Biol

doi: 10.1083/jcb.201907083.

The Bird group together with the Vetter Group and Michael Hiller from the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden have unravelled how clathrin stabilizes microtubules to ensure mitotic spindle stability and efficient chromosome alignment. This function of clathrin is mediated by the recruitment of the microtubule stabilizing protein GTSE1 via adaptor interaction sites on clathrin heavy chains (CHC). Structural analysis reveal that these sites interact directly with clathrin-box motifs on GTSE1. Disruption of the Clathrin-GTSE1 interaction releases GTSE1 from spindles thereby causing defects in chromosome alignment. 

GTSE1 promotes microtubule stability by inhibiting the activity of the microtubule-destabilizing enzyme MCAK, as shown by Bird et al. in JCB in 2016. Thus, a major mechanism by which clathrin stabilizes microtubules is ultimately inhibition of MCAK.

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