Molecular Biology

Faculty and Research Interests

Katrina Cooper PhDKatrina F. Cooper, PhD

Assistant Professor
Science Center, Room 362
856 566-2887
Fax: 856 566-6291


University of Oxford, Great Britain
D. Phil. Biochemistry 1993

University of Manchester, Great Britain.
Hons. B. Sc. Microbiology 1989

Research Interests

The long-term goal of my research is to elucidate the mechanism by which a cell decides its fate in response to environmental cues. Misinterpretation of these signals can result in the cell choosing the incorrect fate, which, in turn, can lead to neoplasia, i.e. tumor formation. To address this question my laboratory uses the model system Saccharomyces cerevisiae (bakers yeast) to understand how cells choose to live or die via programmed cell death following stress. To execute this we focus on a conserved tumor suppressor protein called cyclin C. Cyclin C is a transcription factor which, accompanied by its cyclin dependent kinase 8 (Cdk8), represses many stress response genes. However, following exposure to external reactive oxygen species cyclin C relocates from the nucleus to the outer membrane of the mitochondria where it is required for stress-induced mitochondrial fission and PCD. My laboratory is currently focused on understanding the mechanism by which the stress signal is transmitted to cyclin C as well as deciphering the molecular switch mechanism that releases cyclin C from the nucleus. The nuclear-cytoplasmic translocation of cyclin C is conserved from yeast to man. Thus the information gained from our studies on cyclin C in yeast will translate directly to understanding how this tumor suppressor functions in humans.

RELEVANT Publications

1. Wang K, Yan R, Cooper KF, Strich R." Cyclin C mediates stress-induced mitochondrial fission and apoptosis." Mol Biol Cell. 2015 Mar 15;26(6):1030-43. doi: 10.1091/mbc.E14-08-1315. Epub 2015 Jan 21.


2. Jin, C., Strich, R. and Cooper, K.F. (2014) "Slt2p phosphorylation induces cyclin C nuclear to cytoplasmic translocation in response to oxidative stress." Mol Biol Cell Epub Feb. 19: 2014; doi:10.1091/mbc.E13-09-0550


3. Khakhina S., Cooper K.F, Strich R. (2014) "Med13p prevents mitochondrial fission and programmed cell death in yeast through nuclear retention of cyclin C." Mol Biol Cell. Sep 15;25(18):2807-16


4. Cooper, K. F, Khakhina, S,. Kim, S. K. and Strich, R. (2014)" Stress-Induced Nuclear to Cytoplasmic Translocation of Cyclin C Promotes Mitochondrial Fission in Yeast." Dev Cell 28: 161–173.


Highlighted in Dev Cell, Volume 28, Issue 2, 112-114, 27 January 2014 “Cyclin C: An Inducer of Mitochondrial Division Hidden in the Nucleus” by Yoshihiro Adachi and Hiromi Sesaki.


5. Tan GS, Lewandowski R, Mallory MJ, Strich R, Cooper K.F. (2013)" Mutually dependent degradation of Ama1p and Cdc20p terminates APC/C ubiquitin ligase activity at the completion of meiotic development in yeast." Cell Div. Jul 1;8(1):9.


6. Cooper, K. F., Scarnati, M. S., Krasley, E., Mallory, M. J., Jin, C., Law, M. J. and Strich, R. (2012) "Oxidative stress-induced nuclear to cytoplasmic relocalization is required for Not4-dependent cyclin C destruction." (2011) J.Cell Sci 125: 1015-1026.


7. Tan, G.S., Magurno, J. and Cooper K.F. (2010)" Ama1p activated anaphase promoting complex regulates the destruction of Cdc20p during meiosis II." Mol Biol Cell. 22: 315-326 2011.



1) Strich, R. and Cooper, K.F. (2014) "The dual role of cyclin C connects stress regulated gene expression to mitochondrial dynamics." Microbial Cell, 1 (10) 318-324. Cover Issue.

2) Cooper, K. F., and Strich, R. Cell Div. (2011) "Meiotic control of the APC/C: similarities & differences from mitosis." Cell Div 6:16 (senior and 1st author). Cell Div 6: 16.

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