University of Arizona Cancer Center member Gregory Rogers, PhD, will once again see his work featured in the Journal of Cell Biology, this time highlighting his laboratory’s groundbreaking work in the field of chromosome territories.
His paper, titled “SCFSlimb ubiquitin ligase suppresses condensin II–mediated nuclear reorganization by degrading Cap-H2,” will be published in the April 1, 2013 edition.
“Over the last three or four years, we’ve seen many high-profile researchers using cutting-edge techniques to publish research describing and observing chromosome territories,” Dr. Rogers said. “We’re still not entirely sure what these chromosome territories can do, and we won’t know the answer until we can turn them on and off. We believe we’ve found one mechanism to do just that.”
Dr. Rogers is an assistant professor of cellular and molecular medicine at The University of Arizona, and has been a University of Arizona Cancer Center member since 2008. His research focuses primarily on the molecular mechanisms cells use to maintain stability of their genomes, as genomic instability can promote the production or formation of tumors.
The initial groundwork for this research was laid roughly eight years ago, when Dr. Rogers was studying the SCFSlimb gene as a post-doctoral student at the University of North Carolina. When he brought his research to the University of Arizona, he collaborated with former UACC member and current Dartmouth professor Giovanni Bosco, who was studying the regulatory compound, Cap-H2.
“It was a completely serendipitous series of events,” Dr. Rogers said, adding that he continues to collaborate with Dr. Bosco in this specific field of study.
What they found was that a mutation in the SCFSlimb gene caused cells to have too much condensin II activity, leading to cell instability and a distortion in the nuclear envelope — a set of circumstances that may leave a cell vulnerable to diseases such as Progeria (a rare genetic condition that produces rapid aging in children).
“Cells put a great deal of energy into maintaining a normal nuclear state,” Dr. Rogers said. “If you inhibit a regulatory gene like SCFSlimb, you see the formation of these very dramatic chromosome territories. This is the first time we’ve been able to go beyond simply observing chromosome territories to actually manipulating them. The potential scientific impacts of this new-found ability to turn chromosome territories on and off are very exciting.”
Currently, the research shows no direct link to tumor formation, but Dr. Rogers believes it’s only a matter of time before that link is discovered.
“I have no doubt that when we start looking at chromosome territories in cancer, they will be altered in some way, directly impacting gene expression patterns,” Dr. Rogers said.
Dr. Rogers was previously featured in the Journal of Cell Biology with his article, titled “The Protein Phosphatase 2A regulatory subunit Twins stabilizes Plk4 to induce centriole amplification,” the first research paper that Dr. Rogers published since establishing his own lab at the Cancer Center more than four years ago. This paper helped Dr. Rogers land his first major grant in April 2012, courtesy of the National Science Foundation, to further his research on organelle biogenesis. The $660,000 grant will continue through 2016.
In 2009, Dr. Rogers published a manuscript, also in the Journal of Cell Biology, identifying the tumor suppressor serine/theonine kinase and PLK4 as a licensing factor that localizes to the mitotic centrioles and “primes” them to duplicate later during the cell cycle.
The Journal of Cell Biology is an international peer-reviewed journal owned by The Rockefeller University and published by The Rockefeller University Press.
-Nick Prevenas, March 27, 2013