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

Artikel i vetenskaplig tidskrift
Författare A. Rondelet
Y. C. Lin
D. Singh
A. T. Porfetye
H. C. Thakurle
A. Hecker
P. Brinket
N. Schmidt
S. Bendre
F. Muller
L. Mazul
Per O Widlund
T. Bange
M. Hiller
I. R. Vetter
A. W. Bird
Publicerad i Journal of Cell Biology
Volym 219
Nummer/häfte 2
Sidor 29
ISSN 0021-9525
Publiceringsår 2020
Publicerad vid Institutionen för biomedicin
Sidor 29
Språk en
Länkar dx.doi.org/10.1083/jcb.201907083
Ämnesord n-terminal domain, centromere-associated kinesin, chromosome, congression, bac transgeneomics, kinetochore fibers, multiple sites, xenopus eggs, d-tacc, protein, dynamics, Cell Biology
Ämneskategorier Biokemi och molekylärbiologi

Sammanfattning

Clathrin ensures mitotic spindle stability and efficient chromosome alignment, independently of its vesicle trafficking function. Although clathrin localizes to the mitotic spindle and kinetochore fiber microtubule bundles, the mechanisms by which clathrin stabilizes microtubules are unclear. We show that clathrin adaptor interaction sites on clathrin heavy chain (CHC) are repurposed during mitosis to directly recruit the microtubule-stabilizing protein GTSE1 to the spindle. Structural analyses reveal that these sites interact directly with clathrin-box motifs on GTSE1. Disruption of this interaction releases GTSE1 from spindles, causing defects in chromosome alignment. Surprisingly, this disruption destabilizes astral microtubules, but not kinetochore-microtubule attachments, and chromosome alignment defects are due to a failure of chromosome congression independent of kinetochore-microtubule attachment stability. GTSE1 recruited to the spindle by clathrin stabilizes microtubules by inhibiting the microtubule depolymerase MCAK. This work uncovers a novel role of clathrin adaptor-type interactions to stabilize nonkinetochore fiber microtubules to support chromosome congression, defining for the first time a repurposing of this endocytic interaction mechanism during mitosis.

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