Mechanical Engineering Fall Seminar Series: Class 530.803

November 9, 2017 @ 3:00 pm – 4:00 pm
210 Hodson Hall

“p53 dynamics and the DNA damage response in single cells”

Presented by Dr. Eric BatchelorNational Institutes of Health

The transcription factor p53 is upregulated in response to numerous cellular stresses, including various forms of DNA damage. When activated, it can regulate the transcription of over a hundred genes, affecting a cell’s ability to repair damage, divide, or undergo programmed cell death if damage is too great. Single-cell level analysis of the p53 regulatory circuit revealed that p53 exhibits complex dynamical behavior. In response to one form of activating stress, DNA double strand breaks, p53 levels can accumulate in oscillatory pulses. The amplitude and the duration of individual p53 pulses within a cell and between cells is independent of the dose of the DNA damaging agent; however, the number of pulses increases with higher doses of damage. In this seminar, I will discuss recent work from my lab in which we determine functional consequences of p53 oscillations in terms of the regulation of transcription and cell fate decisions.

Dr. Batchelor received his B.S. in Physics from Villanova University. He obtained his M.S. and Ph.D. in Physics from the University of Pennsylvania, where he studied two-component signal transduction in bacteria. He pursued postdoctoral training in the Department of Systems Biology at Harvard Medical School, where he studied p53’s dynamical response to DNA damage. Dr. Batchelor heads the LP’s Systems Biology section. His research combines experimental and computational approaches to understand how individual cells process information about their intracellular state and extracellular environment, and how they use that information to affect appropriate responses. His current work focuses on the tumor suppressor protein p53, an important regulator in the response to DNA damage. Dr. Batchelor aims to understand how p53 functions in healthy cells, as well as how the p53 network is deregulated in cancer cells.

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