300 North Washington St.
Gettysburg, PA 17325-1400
BA Gettysburg College, 1980
MS University of Minnesota, 1983
PhD University of Minnesota, 1989
Eukaryotic molecular genetics, cancer biology, DNA damage responses, meiosis
Dr. James is a molecular biologist and geneticist. He is a member of the Biology and Biochemistry and Molecular Biology (BMB) programs.
Bio 351 - Molecular Genetics
Bio/CS 251 - Introduction to Bioinformatics
Bio 102 - Biological Basis of Disease
Dr. James and his students use techniques of genetic engineering, genetics, and cell biology to investigate how normal cells “get it right” each time they divide to form new cells, and why cancer cells “get it wrong” every time. In this endeavor, Dr. James uses the filamentous fungus Aspergillus nidulans as a tool for studying the mechanisms that cells employ to protect themselves from cancer-causing DNA damage. In particular, he is working to understand how cells cope with broken chromosomes, the most dangerous and carcinogenic form of DNA injury. In a normal somatic cell, for example, just one double-strand break (DSB) is lethal if unrepaired, and can lead to cancer if repaired imprecisely. Paradoxically, germline cells that undergo meiosis (to form sperm and egg) must deliberately induce chromosome breaks in order to promote crossing over, or genetic exchange, between homologous chromosomes. In the absence of these self-inflicted chromosome breaks, meiosis fails and gametes cannot be formed. The James laboratory is currently exploring the role of two genes, called nimO (never-in-mitosis) and snoA (suppressor-of-nimO), which are critical for repairing chromosome breaks that occur accidentally in normal somatic cells. These same genes also play important roles in meiosis, where they appear to control both the induction and repair of programmed DSBs that are necessary for genetic exchange and subsequent formation of gametes.
Dr. James works with students during the academic year and summers to unravel the interplay of these two genes to control meiosis and the response to DNA damage.