The Spindle Assembly Checkpoint (SAC) is a surveillance mechanism that ensures accurate segregation of chromosomes into two daughter cells. BubR1, a key component of the SAC, play also a role in the mitotic timing since depletion of BubR1 leads to an accelerated mitosis. We previously found that, unlike what was reported in mammalian cells, mutation of the KEN1-box domain of Drosophila BubR1 (bubR1-KEN1 mutant) that affects the binding of BubR1 to Cdc20, the activating co-factor of the APC/C, did not accelerate the mitotic timing despite resulting in a defective SAC. Here, we show that a mutation in a novel Drosophila short sequence (bubR1-KAN mutant) leads to an accelerated mitotic timing as well as SAC failure. Moreover, our data indicate that the level of Fzy, the Drosophila homolog of Cdc20, recruited to kinetochores is diminished in bubR1-KEN1 mutant cells and further diminished in bubR1-KAN mutant cells. Altogether, our data show that this newly identified Drosophila BubR1 KAN motif is required for a functional SAC and suggest that it may play an important role on Cdc20/Fzy kinetochore recruitment.
- Received August 10, 2016.
- Accepted October 7, 2016.
- © 2016. Published by The Company of Biologists Ltd
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