Polo kinase and mitotic controls

A postdoctoral fellowship is available to study the mitotic functions of mammalian polo kinase Plk1 and its novel substrate, PBIP1. PBIP1 is a kinetochore protein, whose deregulation contributes to the promotion of various cancers in humans. Our results showed that PBIP1 is critical for the recruitment of Plk1 to the kinetochores and the spindle checkpoint signaling, and absence of PBIP1 function leads to chromosome segregation defect and aneuploidy. Analyses of the Plk1-PBIP1 interaction revealed that PBIP1 interacts with the polo-box domain of Plk1 in a manner that requires phosphorylation of PBIP1 on the T78 residue. Small phospho-T78 peptides, but not the corresponding non-phospho peptides, specifically interacted with Plk1, thus providing a promising lead for the isolation of anti-Plk1 therapeutic agents.

Projects include, but are not limited to, mechanisms of Plk1-PBIP1 interaction and Plk1-dependent PBIP1 degradation in late mitosis, characterization of novel PBIP1-interacting proteins, role of PBIP1 during tumorigenesis, and generation of PBIP1 knock-in and transgenic mice. Please visit http://home.ccr.cancer.gov/metabolism/kleeccr.htm for more information. Expertise in biochemistry, cell biology, and/or mouse experimental models will be preferred. Salary starts at $46,200 for a fellow with no previous postdoctoral training. Please send CV to Dr. Kyung S. Lee (kyunglee@mail.nih.gov), National Institutes of Health, Bethesda, MD, U. S. A.