Molecular Biology

Faculty and Research Interests

Randy S Strich, PhDRandy Strich, PhD

Science Center 354


University of Illinois at Urbana, IL
PhD (Microbiology) , 1986

University of Illinois at Urbana, IL
MS (Microbiology) , 1983

University of Pennsylvania, PA
BA (Biology) , 1980



Many anti-cancer therapies kill tumor cells by elevating ROS to levels sufficient to trigger apoptosis. However, this approach will fail if ROS levels are not increased enough in tumor cells due to poor drug delivery or if the treatment elevates ROS levels above the toxicity threshold in normal cells. Therefore, the ability to manipulate the ROS sensitivity thresholds may allow more effective use of anticancer strategies. Cellular damage in many forms induces mitochondrial fragmentation, an early step in the programmed cell death pathway. This mitochondrial dynamics play an important role in setting the threshold for apoptotic initiation. Studies in my laboratory and others have found that preventing mitochondrial fragmentation protects cells from stress-induced apoptosis. My laboratory focuses on the role played by a protein (cyclin C) in orchestrating stress-induced hyper-fission and apoptosis. Unlike other cyclin-Cdks that control the cell cycle, cyclin C, and its cyclin dependent kinase Cdk8, regulate transcription through direct association with the RNA polymerase II holoenzyme. However, we discovered a second function for cyclin C that occurs outside the nucleus. In response to cellular damage, a portion of cyclin C translocates to the mitochondria where it associates with components of the fission machinery. Using knockout (CCNC-/-) mammalian and yeast cells, we find that cyclin C is required for stress-induced mitochondrial hyper-fission and apoptosis. Consistent with a tumor suppressor role for cyclin C, we found that CCNC ablation dramatically accelerates hyperplasia in a mouse thyroid tumor model. Currently, my laboratory is exploiting yeast, mammalian cell culture and mouse knockout systems to study the role of cyclin C in preventing tumor progression. Our ability to jump back and forth between the yeast and mammalian systems provides an excellent platform to elucidate the role cyclin C plays in both mitochondrial fission and PCD execution.

Our second area of research is directed toward understanding the switch between mitotic cell division and meiotic differentiation in the budding yeast. Meiosis is a specialized, highly conserved process designed to redistribute the genetic material and produce haploid cells capable of sexual reproduction. My laboratory investigates two important questions in controlling meiotic development. First, we are investigating the molecular switch between mitosis and meiosis to determine how the cell executes this change in cell fate. Our work analyzes the targeted destruction of transcriptional repressors required for meiotic gene transcription. This degradation is triggered by a novel signal that includes acetylation of the repressor which makes it a substrate for the anaphase promoting complex ubiquitin ligase. In addition, we are examining the interplay between transcription factor regulation and chromatin remodeling enzymes that mediate the transient transcription expression profiles observed during meiosis.


1. Mallory, M.J., M.J. Law, L.E. Buckingham, and R. Strich, The Sin3p PAH domains provide separate functions repressing meiotic gene transcription in Saccharomyces cerevisiae. Eukaryot Cell, 2010. 9(12): p. 1835-44. PMID: 20971827

2. Cooper, K.F. and R. Strich, Meiotic control of the APC/C: similarities & differences from mitosis. Cell Div, 2011. 6(1): p. 16. PMID: 21806783

3. Cooper, K.F., M.S. Scarnati, E. Krasley, M.J. Mallory, C. Jin, M.J. Law, and R. Strich, Oxidative-stress-induced nuclear to cytoplasmic relocalization is required for Not4-dependent cyclin C destruction. J Cell Sci, 2012. 125 p. 1015-26. PMID: 22421358

4. Mallory, M.J., M.J. Law, D.E. Sterner, S.L. Berger, and R. Strich, Gcn5p-dependent acetylation induces degradation of the meiotic transcriptional repressor Ume6p. Mol Biol Cell, 2012. 23(9): p. 1609-17. PMID: 22438583

5. Jin, C., A.V. Parshin, I. Daly, R. Strich, and K.F. Cooper, The cell wall sensors Mtl1, Wsc1, and Mid2 are required for stress-induced nuclear to cytoplasmic translocation of cyclin C and programmed cell death in yeast. Oxid Med Cell Longev, 2013. 2013: p. 320823. PMID: 24260614

6. Law, M.J., M.J. Mallory, R.L. Dunbrack, Jr., and R. Strich, Acetylation of the transcriptional repressor Ume6p allows efficient promoter release and timely induction of the meiotic transient transcription program in yeast. Mol Cell Biol, 2014. 34: p. 631-642. PMID: 24298021

7. Tan, G.S., R. Lewandowski, M.J. Mallory, R. Strich, and K.F. Cooper, Mutually dependent degradation of Ama1p and Cdc20p terminates APC/C ubiquitin ligase activity at the completion of meiotic development in yeast. Cell Div, 2013. 8(9): p. 1-12. PMID: 23816140

8. Cooper, K.F., S. Khakhina, S.K. Kim, and R. Strich, Stress-Induced Nuclear-to-Cytoplasmic Translocation of Cyclin C Promotes Mitochondrial Fission in Yeast. Dev Cell, 2014. 28: p. 161-173. PMID: 24439911

9. Jin, C., R. Strich, and K.F. Cooper, Slt2p phosphorylation is required for the stress-induced cytoplasmic translocation and destruction of the yeast transcriptional repressor cyclin C. Mol Biol Cell, 2014. In Press. PMID: 24554767

10. Wang, K., R. Yan, K. F. Cooper and R. Strich, 2015 Cyclin C mediates stress-induced mitochondrial fission and apoptosis. Mol Biol Cell 26: 1030-1043.

11. Strich, R., 2015 Programmed Cell Death Initiation and Execution in Budding Yeast. Genetics 200: 1003-1014.


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.
Also was featured as Editors Choice in Science Signaling 2014, Vol.7 page-ec33 “Cyclin C Moves Out of the Nucleus” by VanHook, A.M.




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