Xuebiao Yao graduated from the University of California-Berkeley in 1995 followed by a postdoctoral fellowship at University of California-San Diego. He was appointed by the University of Wisconsin-Madison as a tenure-track assistant professor in 1997. In 1998, Dr. Yao was recruited to the University of Science & Technology of China as Cheung Kong Professor. He established the Laboratory of Cellular Dynamics in 1999. The research interest in Dr. Yao’s laboratory centers on spatiotemporal dynamics of molecular circuitry underlying cell fate plasticity control.
Dr. Yao was recognized by the Natural Science Foundation of China as an Outstanding Young Scientist in 1999 and a co-recipient of a National Medal in 2015 for discovery of a novel cytokine signaling axis. After his establishment of the Laboratory of Cellular Dynamics, Dr. Yao has published more than 100 articles in Cancer Cell, Nat. Rev. Mol. Cell Biol., Nat. Chem. Biol., PNAS, Cell Research etc. He also serves on numerous editorial boards such as J.
Biol. Chem., Cell Discovery, Cell Res.， and associate editors for J. Mol. Cell Biol. and BMC Cell Biol. as well as Keystone Symposium SAB member. He has trained a collection of outstanding young cell biologists in China. Among these trainees, many were recognized as Qing Qian Scholars, Ray Wu Prize and CAS President Awardees.
The inheritance of genetic material depends on the consistent segregation of chromosomes in mitosis. The physical connection between the centromeres and spindle microtubules is orchestrated by the kinetochore, a protein supercomplex assembled onto the centromere. Faithful segregation of chromosomes in mammalian cells requires bi-orientation of sister chromatids, which relies on the sensing of correct attachments between spindle microtubules and kinetochores. Although the mechanisms underlying cyclin-dependent kinase 1 (CDK1) activation, which triggers mitotic entry, have been extensively studied, the regulatory mechanisms that couple CDK1-cyclin B activity to chromosome stability are not well understood. Here, we identified a signaling axis in which Aurora B activity is modulated by CDK1-cyclin B via the acetyltransferase TIP60 in human cell division. CDK1-cyclin B phosphorylates Ser90 of TIP60, which elicits TIP60-dependent acetylation of Aurora B and promotes accurate chromosome segregation in mitosis. Mechanistically, TIP60 acetylation of Aurora B at Lys215 protects Aurora B's activation loop from dephosphorylation by the phosphatase PP2A to ensure a robust, error-free metaphase-anaphase transition. These findings delineate a conserved signaling cascade that integrates protein phosphorylation and acetylation with cell cycle progression for maintenance of genomic stability.