Schematic representation of the domain and degron architecture of Nek2A.
The MR tail is the main contributor for Nek2A ubiquitination. Ubiquitination reactions performed with APC/CCdc20 for Nek2A wild‐type (Nek2AWT) and degron mutants. Nek2AK is the KEN‐box mutant (391KEN393/KAA), Nek2AK/D is the (KEN‐ and D‐box mutant (391KEN393/KAA, 361RKFL364/AKFA), and Nek2AMR is the 443ΔMR mutant.
The APC/C requires the Cdc20 coactivator subunit to ubiquitinate Nek2A. Nek2A ubiquitination reactions performed with the APC/C in the absence and presence of increasing concentrations of Cdc20 using the E2 UbcH10.
The MR tail is essential for Nek2A binding to the APC/C, whereas in contrast Cdc20 is dispensable. Size‐exclusion chromatography peak fractions of APC/C complexes with Nek2A. The input material (13% of total) is indicated (i). Peak fractions are numbered in respect of the chromatograms in Fig
EV1.
Nek2A binding does not stabilize binding of the coactivator subunit Cdc20 to the APC/C and does not compete with cyclin A for binding to the APC/C. Size‐exclusion chromatography peak fractions of APC/C complexes with Nek2A.
Top: Cylinder representation of the APC/C–Nek2A complex structure. The TPR lobe subunits are highlighted: Apc8 (cyan), Apc6 (pink), Apc3 (yellow) and Apc7 (green). The platform subunits and the small subunits from the TPR lobe are shown in transparency. Bottom: cryo‐EM density of the Nek2AMR tail dipeptide and details of the Nek2AMR tail (orange) binding site on Apc8A.
Details of the IR tail of Cdc20MCC (orange) bound to Apc8A in APC/CMCC‐closed. This is the same site as the Nek2AMR tail binding site shown above. Shown is the cryo‐EM density for the Cdc20MCC IR tail and contacting residues of Apc8A.