Faculty and Research Interests
Randy 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
Our research focuses on two main questions. First, many current anti-cancer drug strategies attempt to generate sufficient cellular damage to induce programmed cell death (PCD). However, many pathways that trigger PCD utilize p53, which is mutated in over half of the tumors examined. Therefore, it is important to identify new strategies by which to attack this problem. Our results revealed that cyclin C is previously unknown PCD inducer in both yeast and mammalian systems. Unlike other cyclin-Cdk kinases, cyclin C-Cdk8 does not control cell cycle progression. Rather, cyclin C and Cdk8 are transcription factors. However, we have discovered a new role for cyclin C in mediating stress-induced mitochondrial fission and PCD independent of Cdk8. Our current research is focused on understanding how cyclin C controls PCD and how this activity can be manipulated to aid in killing cancer cells. We have expanded these studies into a cyclin C knockout mouse system to determine whether this protein influences drug sensitivity and tumor development using in vivo cancer models.
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., K. F. Cooper, and R. Strich. 2007. Meiosis-specific destruction of the Ume6p repressor by the Cdc20-directed APC/C. Mol Cell 27:951-61.
2. Cohen, T., M. Mallory, R. Strich, and T. Yao. 2008. Hos2p/Set3p deacetylase complex signals secretory stress through the Mpk1p cell integrity pathway. Eukaryot Cell. 7:1191-9.
3. Cooper, K. F., M. J. Mallory, V. Guacci, K. Lowe, and R. Strich. 2009. Pds1p is required for meiotic recombination and prophase I progression in Saccharomyces cerevisiae. Genetics 181:65-79.
4. Mallory, M., M. Law, L. Buckingham, and R. Strich. 2010. The Sin3p PAH Domains Provide Separate Functions Repressing Meiotic Gene Transcription in Yeast. Euk. Cell 9:1835-1844.
5. Strich, R., S. Khakhina, and M. J. Mallory. 2010. Ume6p is Required for Germination and Early Colony Development of Yeast Ascospore. FEBS Yeast 11:104-113.
6. Cooper, K. F., and R. Strich. 2011. Meiotic control of the APC/C: similarities & differences from mitosis. Cell Div 6:16.
7. Strich, R. 2011. Meiotic, cryptic, and stable unannotated transcripts: noncoding RNAs add to the epigenetic tool box controlling meiotic development. Proc Natl Acad Sci U S A 108:891-2.
8. Cooper, K. F., E. Krasley, M. Scarnati, M. J. Mallory, C. Jin, M. J. Law, and R. Strich. 2012. Stress-induced cyclin C destruction requires cytoplasmic relocalization and the Not4 ubiquitin ligase. J. Cell Sci. In Press.