The authors came to this conclusion after identifying mutants that were dependent on high Plo1 expression for their survival. One of the mutants made a Cdc23 protein that interacted poorly with Plo1, a deficit that May et al. suggest is overcome by excess Plo1. Following up on this clue, May et al. mapped the Plo1–Cdc23 interaction to the noncatalytic domain of Plo1 and the TPR domain of Cdc23.
The APC...
The Rockefeller University Press
2002
The Rockefeller University Press
2002
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