Figure 7: Working model of Diaph3 function in the spindle checkpoint.
From: Lack of Diaph3 relaxes the spindle checkpoint causing the loss of neural progenitors
(a) Molecular interactions between Diaph3, CPC and SAC proteins during cell division. Documented interactions are depicted in red and new findings are shown in purple. Diaph3 localizes with CPC proteins and co-immunoprecipitates with Survivin and BubR1. (b) Absence of Diaph3 probably disrupts the Diaph3–APC–Eb1 complex, which interacts with and stabilizes the CPC complex at the spindle–kinetochore interface. Loss of Diaph3 impairs the localization of CPC proteins and the ability of dividing cells to activate the SAC. Diaph3-deficient cells fail to accumulate BubR1, leading to slippage to anaphase and mitotic catastrophe and/or cell death of aneuploid progeny.
