John J. Tyson

Portrait of John J. Tyson

John J. Tyson (born December 12, 1947, in Abington, Pennsylvania) is an American systems biologist and mathematical biologist who serves as University Distinguished Professor of Biology at Virginia Tech, and is the former president of the Society for Mathematical Biology.[1] He is known for his research on biochemical switches in the cell cycle, dynamics of biological networks and on excitable media.

Tyson earned a bachelor's degree in chemistry from Wheaton College, and received his Ph.D in chemical physics from the University of Chicago. After postdoctoral research at the Max Planck Institute for Biophysical Chemistry, a temporary position teaching mathematics at the University at Buffalo, and another post doctorate at the University of Innsbruck for Biochemistry and Experimental Cancer Research, he joined the Virginia Tech faculty in 1978 and is currently a University Distinguished Professor in Biological Sciences. He was president of the Society for Mathematical Biology for 1993–1995, and served as co-editor-in-chief of the Journal of Theoretical Biology from 1995 to 2004.[1]

Research

Since receiving his PhD in chemical physics at the University of Chicago in 1973, John Tyson has been studying temporal and spatial organization in chemical, biochemical and biological systems. Recently he has focused on the macro-molecular reaction networks that process information in living cells and initiate appropriate responses in terms of cell growth, division and death. He represents the dynamics of these reaction networks in terms of mathematical equations, using computer simulations to work out the precise behavior to be expected of the network. By comparing simulations with experimental data, the computer models can be tested, refined and developed, eventually, into tools for accurate predictions of the physiological responses of healthy and diseased cells.[2]

In John J. Tyson's laboratory they study biological systems from a rigorous mathematical perspective, and build realistic models that help gain a deeper understanding of the physiology. Most of their work is on the mechanism of cell cycle control as seen in budding yeast, fission yeast, Xenopus embryos and egg extracts, Drosophila embryos and mammalian cells.

Tyson also worked in chemical kinetics studying oscillations, bistability, traveling' waves, and chaotic behavior in chemical reaction systems.

The unifying theme of the research is the problem of spatial and temporal organization in chemical, biochemical and biological systems. What mechanisms keep time in these various domains? How is spatial information communicated and utilized? How do the molecular regulatory mechanisms of living cells process information and initiate appropriate responses in terms of cell growth, division and death?[3]

John Tyson has published several dynamical models of cell decision making systems in cancer including Estrogen Receptor Signaling, Unfolded Protein Response (UPR) and Autophagy.[4][5][6]

Notable Achievements and Recognition

John has worked closely with high profile individuals within the field of cell biology. Cell Cycle Control by a Minimal Cdk Network was written by John in tandem with Claude Gerard, Damien Coudreuse, and Béla Novák. The paper has been highly cited and takes a critical look at the possible origin of the eukaryotic cell and how the minimal cdk network can apply to larger complex cells like those found in humans. John has been featured on television for the annual meeting of the society of cell biology in 2013, as well as being featured on the National Institute of General Medical Sciences website.

Publications

John Tyson's most cited paper, Steady states and oscillations in the p53/Mdm2 network, focuses on the activation of p53 and the genetic integrity of a cell, and how p53 activity does not increase steadily with genetic damage but rather fluctuates in an oscillatory fashion. He and B. Novak developed a mathematical model of p53 oscillations based on positive and negative feedbacks in the p53/Mdm2 network. According to the model, the system reacted to DNA damage by moving from a stable steady state into a region of stable limit cycles. Oscillations in the model are born with large amplitude, which guarantees an all-or-none response to damage. As p53 oscillates, damage is repaired and the system moves back to a stable steady state with low p53 activity. The model reproduced experimental data in quantitative detail.[7]

In an interview published by the Taylor and Francis Group, An interview with Dr. John J. Tyson on his highly cited paper published in Cell Cycle,[2] Tyson talks about the publication and its applications to the field of computational biology.

Question and Answer excerpt from the interview:

Did you expect your paper to become highly cited, or is this surprising to you?

"Maybe not so surprising after all, given that this was the first model proposed to explain a novel phenomenon that involves a superstar protein such as p53."[2]

John Tyson currently has 141 publications on studies which topics include:[8]

Awards

Membership and Offices in Professional Organizations

References

  1. 1 2 Curriculum vitae: John J. Tyson, Virginia Tech, retrieved 2015-10-28.
  2. 1 2 3 "An interview with Dr. John J. Tyson on his highly cited paper published in Cell Cycle". Cell Cycle. 8 (20): 3261–3261. 2009-10-15. doi:10.4161/cc.8.20.10189. ISSN 1538-4101. PMID 19823016.
  3. ↑ "Tyson Lab - Computational Cell Biology". mpf.biol.vt.edu. Retrieved 2015-11-11.
  4. ↑ Tyson, John J.; Baumann, William T.; Chen, Chun; Verdugo, Anael; Tavassoly, Iman; Wang, Yue; Weiner, Louis M.; Clarke, Robert (2011-07-01). "Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells". Nature Reviews Cancer. 11 (7): 523–532. doi:10.1038/nrc3081. ISSN 1474-175X. PMC 3294292Freely accessible. PMID 21677677.
  5. ↑ Tavassoly, I; Parmar, J; Shajahan-Haq, An; Clarke, R; Baumann, Wt; Tyson, Jj (2015-04-01). "Dynamic Modeling of the Interaction Between Autophagy and Apoptosis in Mammalian Cells". CPT: Pharmacometrics & Systems Pharmacology. 4 (4): 263–272. doi:10.1002/psp4.29. ISSN 2163-8306. PMC 4429580Freely accessible. PMID 26225250.
  6. ↑ Chen, Chun; Baumann, William T.; Clarke, Robert; Tyson, John J. (2013-10-11). "Modeling the estrogen receptor to growth factor receptor signaling switch in human breast cancer cells". FEBS Letters. 587 (20): 3327–3334. doi:10.1016/j.febslet.2013.08.022. ISSN 1873-3468. PMC 3893882Freely accessible. PMID 23994522.
  7. ↑ Ciliberto, Andrea; Novak, Béla; Tyson, John J. (2005-03-01). "Steady states and oscillations in the p53/Mdm2 network". Cell Cycle (Georgetown, Tex.). 4 (3): 488–493. doi:10.4161/cc.4.3.1548. ISSN 1551-4005. PMID 15725723.
  8. ↑ "John J Tyson - Google Scholar Citations". scholar.google.com. Retrieved 2015-11-11.
  9. ↑ "Tyson Lab - Computational Cell Biology". mpf.biol.vt.edu. Retrieved 2015-10-31.
  10. ↑ "John J. Tyson - Faculty, Virginia Tech". www.faculty.biol.vt.edu. Retrieved 2015-10-31.

External links

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