期刊
JOURNAL OF CELL BIOLOGY
卷 202, 期 3, 页码 463-478出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201211127
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资金
- Cancer Research UK [C25425/A8722, C24461/A12772]
- Medical Research Council [G0800021]
- Marie Curie Cancer Care program grant
- MRC [MC_U117533887, G0800021] Funding Source: UKRI
- Cancer Research UK [12772, 15182] Funding Source: researchfish
- Medical Research Council [G0800021, MC_U117533887] Funding Source: researchfish
A complex of transforming acidic coiled-coil protein 3 (TACC3), colonic and hepatic tumor over-expressed gene (ch-TOG), and clathrin has been implicated in mitotic spindle assembly and in the stabilization of kinetochore fibers by cross-linking microtubules. It is unclear how this complex binds microtubules and how the proteins in the complex interact with one another. TACC3 and clathrin have each been proposed to be the spindle recruitment factor. We have mapped the interactions within the complex and show that TACC3 and clathrin were interdependent for spindle recruitment, having to interact in order for either to be recruited to the spindle. The N-terminal domain of clathrin and the TACC domain of TACC3 in tandem made a microtubule interaction surface, coordinated by TACC3-clathrin binding. A dileucine motif and Aurora A-phosphorylated serine 558 on TACC3 bound to the ankle of clathrin. The other interaction within the complex involved a stutter in the TACC3 coiled-coil and a proposed novel sixth TOG domain in ch-TOG, which was required for microtubule localization of ch-TOG but not TACC3-clathrin.
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