Research Papers: Chromosome:
Mitosis-specific phosphorylation of Mis18α by Aurora B kinase enhances kinetochore recruitment of polo-like kinase 1
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Minkyoung Lee1,*, Ik Soo Kim1,*, Koog Chan Park2, Jong-Seo Kim3, Sung Hee Baek1, and Keun Il Kim2
1Creative Research Initiatives Center for Chromatin Dynamics, Department of Biological Sciences, Seoul National University, Seoul 08826, South Korea
2Department of Biological Sciences, Cellular Heterogeneity Research Center, Sookmyung Women’s University, Seoul 04310, South Korea
3Center for RNA Research, Institute for Basic Science, Department of Biological Sciences, Seoul National University, Seoul 08826, South Korea
*These authors contributed equally to this work
Keun Il Kim, email: [email protected]
Sung Hee Baek, email: [email protected]
Keywords: Mis18α; Aurora B kinase; PLK1; mitosis-specific phosphorylation; polo box domain
Received: August 06, 2017 Accepted: October 28, 2017 Published: November 27, 2017
Mis18α, a component of Mis18 complex comprising of Mis18α, Mis18β, and M18BP1, is known to localize at the centromere from late telophase to early G1 phase and plays a priming role in CENP-A deposition. Although its role in CENP-A deposition is well established, the other function of Mis18α remains unknown. Here, we elucidate a new function of Mis18α that is critical for the proper progression of cell cycle independent of its role in CENP-A deposition. We find that Aurora B kinase phosphorylates Mis18α during mitosis not affecting neither centromere localization of Mis18 complex nor centromere loading of CENP-A. However, the replacement of endogenous Mis18α by phosphorylation-defective mutant causes mitotic defects including micronuclei formation, chromosome misalignment, and chromosomal bridges. Together, our data demonstrate that Aurora B kinase-mediated mitotic phosphorylation of Mis18α is a crucial event for faithful cell cycle progression through the enhanced recruitment of polo-like kinase 1 to the kinetochore.
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