James Ferrell
Academic Appointments
- Professor, Chemical and Systems Biology
- Member, Stanford Cancer Institute
- Professor, Biochemistry
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 725-0765
Professional Overview
Administrative Appointments
- Associate Chair, Stanford University School of Medicine - Chemical & Systems Biology (2011 - 2012)
- Chair, Stanford University School of Medicine - Chemical & Systems Biology (2006 - 2011)
Professional Education
| B.A.: | Williams College, Physics, Chemistry, Mathematics (1976) |
| Ph.D.: | Stanford University, Chemistry (1984) |
| M.D.: | Stanford University (1986) |
Postdoctoral Advisees
Xianrui Cheng, Sanghoon Ha, Tek Hyung Lee, Silvia Magalhaes Dos Santos, Qiong Yang
Graduate & Fellowship Program Affiliations
Community and International Work
- PRD-1-Day Band Performance, Opening Ceremony, Guangzhou Triennial, Guangzhou, China
Internet Links
Scientific Focus
Current Research Interests
Mitosis and meiosis are certainly among the most spectacular events in all of biology. These processes are brought about by protein kinase complexes consisting of the cyclin-dependent kinase CDK1 (also called Cdc2) and a mitotic cyclin (in animals, an A-type cyclin or a B-type cyclin). The abrupt activation of cyclin-CDK1 at the onset of mitosis, and the abrupt inactivation of cyclin-CDK1 at the metaphase/anaphase transition near the end of mitosis, constitute the climax of the cell cycle and result in the division of one cell into two.
In some circumstances, the eukaryotic cell cycle can be best described as a succession of contingent events. For example, in most somatic cells in culture, cell growth is followed by DNA replication, then more cell growth, then mitotic entry and chromosome congression, then sister chromatid separation and mitotic exit. Entry into a new phase of the cell cycle sometimes depends upon the successful completion of some important event in the previous phase. E.g., the cell cannot begin DNA replication until sufficient growth has occurred, cannot enter mitosis until DNA replication is completed, and cannot initiate sister chromatid separation until congression is achieved. Our goal here is to understand how these switches between phases occur.
In other contexts the cell cycle is better described as an autonomous oscillation. For example, in the early Xenopus embryo, every ~30 minutes CDK1 is activated and this reliable rhythm is maintained even if DNA replication or mitosis is blocked. Our goal here is to understand how this oscillator works.
The approaches we have taken to these questions include quantitative experimental approaches, computational modeling, and the theory of nonlinear dynamics. We hope to understand the design principles of these systems, and perhaps to gain insight into other biological switches and oscillators as well.
Publications
- The Cdk1-APC/C cell cycle oscillator circuit functions as a time-delayed, ultrasensitive switch. Nat Cell Biol. 2013; (5): 519-25
- Bistability, bifurcations, and Waddington's epigenetic landscape. Curr Biol. 2012; (11): R458-66
- Spatial positive feedback at the onset of mitosis. Cell. 2012; (7): 1500-13
- A mechanism for the evolution of phosphorylation sites. Cell. 2011; (4): 934-46
- Modeling the cell cycle: why do certain circuits oscillate? Cell. 2011; (6): 874-85
- Ultrasensitivity in the Regulation of Cdc25C by Cdk1. Mol Cell. 2011; (3): 263-74
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