Julia P. Cooper, Ph.D.
Chromosome ‘linearity’ is so universal among eukaryotes that we assume it to be evolutionarily advantageous. Nonetheless, formidable challenges are presented by linear chromosome ends, as their resemblance to damage-induced DNA breaks makes them vulnerable to degradation and end-joining pathways that provoke aging or cancer. Julie Cooper’s laboratory studies how telomeres protect chromosome integrity, as well as alternative strategies for chromosome end protection in the absence of canonical telomeres. The lab has also discovered unanticipated roles of telomeres in controlling both spindle and centromere assembly during meiosis. These studies are prompting a re-examination of the roles played by specific microenvironments within the nucleus
1) telomeres, 2) centromeres, 3) DNA damage response, 4) meiosis, 5) chromatin structure and replication, 6) telomerase
We study the mechanisms by which chromosome integrity is maintained starting at the telomere, the nucleoprotein complex that forms the end of the chromosome. Our lab focuses on how telomeres protect chromosomes from degradation and fusion, as well as alternative strategies for chromosome end protection in the absence of canonical telomeres. We also study the newly emerging roles of telomeres in controlling both spindle and centromere assembly during meiosis. Most of our studies utilize fission yeast, a versatile model system with telomeres and other heterochromatic regions that are highly conserved with those of human. Telomeres protect our genomes and choreograph chromosome movements; they affect a range of biological processes from cancer avoidance to healthy gamete formation. They prevent the degradation and fusion of chromosome ends and ensure that natural chromosome ends do not elicit the cell-cycle arrest pathways that respond to damage-induced DNA breaks. Telomeres are a particular focus of our research on tumorigenesis (which is associated with genomic instability and telomerase activation) and aging (which is accompanied by a progressive decline in telomere length). However, the complete repertoire and underlying mechanisms of telomere function are not yet understood. The telomeres of fission yeast, the model system we use most in our lab, are remarkably similar to those of humans but provide precise genetic manipulability. Concepts we have developed by studying fission yeast telomeres have repeatedly been shown to predict observations in mammals.
Topics we are exploring include the cell-cycle regulation of telomere function, the fascinating roles taken on by telomeres in controlling spindle formation and centromere assembly during meiosis, and surprising ways in which some cells (such as telomerase-minus cancer cells) can survive in the absence of canonical telomeres.
Selected Key Publications
- Nature. 467: 223-7, 2010. [ Journal Article ]
- Mol Cell. 33: 559-69, 2009. [ Journal Article ]
- Cell. 130: 113-26, 2007. [ Journal Article ]
- Curr Opin Cell Biol. 26: 123-31, 2014. [ Journal Article ]
- EMBO Rep. 14: 252-60, 2013. [ Journal Article ]
Dr. Julia Cooper earned her B.S. in biology from Emory University and received her Ph.D. in biochemistry/biophysics/genetics from the University of Colorado Health Sciences Center. She completed her postdoctoral training at the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases (now NIDDK and NIAMS), the University of Colorado at Boulder (Howard Hughes Medical Institute); and the Imperial Cancer Research Fund, London (now Cancer Research UK).
|Manasi Sadanand Apte Ph.D.||Postdoctoral Fellow (Visiting)|
|Adenrele M. Gleason Ph.D.||Postdoctoral Fellow (CRTA)|
|Haitong Hou Ph.D.||Research Fellow|
|Hirohisa Masuda Ph.D.||Research Fellow|
|Rishi Kumar Nageshan Ph.D.||Postdoctoral Fellow (Visiting)|
|Raquel Ortega||Postbaccalaureate Fellow (CRTA)|
|Nadeem Shaikh Ph.D.||Postdoctoral Fellow (Visiting)|
|Rahul Rajan Thadani Ph.D.||Postdoctoral Fellow (Visiting)|