Fig. 7: Schematic model. | Nature Communications

Fig. 7: Schematic model.

From: The RepID–CRL4 ubiquitin ligase complex regulates metaphase to anaphase transition via BUB3 degradation

Fig. 7

RepID (structural DCAF) brings CRL4 on chromatin during interphase. BUB3 is localized to PML-NB, which protects BUB3 from degradation by CRL4CDT2. In RepID-deficient cells, BUB3 degradation is compromised even when PML-NB levels are decreased because chromatin-bound CRL4 are low. During mitosis, RepID recruits CRL4 on chromosome and binds to the kinetochore-localizing BUB3. While RepID is dissociated from CRL4, mitotic spindle-localizing RBBP7 (catalytic DCAF) is incorporated into CRL4 during metaphase. CRL4RBBP7-dependent degradation of BUB3 promotes dissociation of SAC, resulting in CDC20–APC/C interaction and anaphase initiation. RepID-deficient cells exhibit no changes in function, expression, or localization of RBBP7 and BUB3. Prolonged metaphase–anaphase transition by defective BUB3 degradation in RepID-deficient cells is due to a decrease of CRL4 on mitotic chromosomes, leading to increased sensitivity to PTX treatment.

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