Our Science – Rong Website

Yikang Rong, Ph.D.

Laboratory of Biochemistry and Molecular Biology Head, Eukaryotic Genome Maintenance Unit Investigator National Cancer Institute Building 37, Room 6056D Bethesda, MD 20892 Phone:   301-451-8335 Fax:   301-435-3697 E-Mail:   rongy@mail.nih.gov

Biography

Dr. Yikang Rong received his Ph.D. in genetics from the University of Utah in 1998.

Research

The fruitfly Drosophila melanogaster is one of the best genetic model organisms for a large number of research areas in modern biology. However, one of the most useful genetic tools has been prominently missing for Drosophila, that is the ability to target specific genes for mutation by homologous recombination. Gene targeting has, for more than 20 years, allowed yeast and mouse researchers to introduce specific mutations into essentially any gene. Such a tool is especially important for gene function studies in organisms with a completely sequenced genome. Dr. Rong was the main driving force for the recent development of a gene targeting method in Drosophila. This method has allowed Drosophila researchers worldwide to successfully mutate many different loci that were not previously identified in traditional mutant screens.

Dr. Rong’s group is interested in studying the mechanisms for DNA double-strand break (DSB) repair in Drosophila. To facilitate such a study, Dr. Rong has introduced a site-specific DSB system into Drosophila in which one can control the position of the break, the number of breaks, the timing of the breakage, and the genomic environment surrounding the break. Using this system, Dr. Rong was able to provide evidence suggesting that genomic structure around the DNA break dictates the choice of not only the repair mechanism but also the template for repair. A goal of the lab is to combine the power of the site-specific breakage system and the gene targeting method to elucidate the function of gene products involved in the repair of these DNA lesions.

Dr. Rong's group is also interested in studying the cellular response to DNA damage. A eukaryotic cell uses multiple mechanisms to respond to DNA damage. As a part of the response, the cell stop the progression of various cell cycle programs to ensure proper repair of the damage or to induce cell death so that cells that have been damaged beyond repair can be eliminated. These responses to damage are partly controlled by the p53 tumor suppressor, the ATM checkpoint kinase and the Mre11 protein complex. Dr. Rong's group has successfully generated knockout mutants of p53, ATM and members of the Mre11 complex. Research is on going to characterize the mutant phenotypes.

The work of Dr. Rong’s group should contribute to a better understanding of how eukaryotic organisms maintain the physical integrity of their genomes, and shed lights on how genome instability could give rise to human cancer.

This page was last updated on 6/12/2008.