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GEN’s editorial staff interviews life science academic and biotech industry leaders on important research, technology, and trends. These podcasts will keep you informed with all the important details you need.
While most of the non-coding DNA in the human genome is junk, some of it, known as regulatory DNA, is used to help genes turn on and off. Now comes an unexpected finding from researchers at the Johns Hopkins School of Medicine. They recently reported that regulatory DNA, which contributes to inherited diseases like Parkinson’s or mental disorders, may be more abundant than we realize.
During this week's podcast, Dr. Andrew McCallion talks about how he and his team came to this conclusion. He gives his thoughts on why current computer programs that scan the human genome looking for regulatory DNA might be missing more that 60 percent of these key DNA regions. Although Dr. McCallion agrees that sequence conservation is a good method to begin finding regulatory elements, he presents his case on why to fully understand our genome we need other approaches to locate the missing regulatory elements. Dr. McCallion provides the details of his team's study and on the use of zebrafish in the research project. He also discusses the implications of this work for further human genome research.
Listen to the podcast then return to the blog to give your thoughts on the following question:
If non-coding regulatory DNA does indeed turn out to be much more abundant in the human genome, what are the implications for genomic research?
Or, if you prefer, post your own topic on the biotech industry subject of your choice. Please share your opinions and observations.
Dr McCallion was trained in genetics at the University of Glasgow (Scotland, UK), and received his Ph.D. in 1998. He received his Post-Doctoral training with Dr Aravinda Chakravarti in the McKusick Nathans Institute of Genetic Medicine at Johns Hopkins University and focused on the genetic dissection of Hirschsprung Disease (HSCR). He has published widely on the resulting work, which included the synthesis of the first clinically accurate mouse model of a multigenic disease (HSCR) and has authored book chapters in such texts as: The molecular and Metabolic basis of inherited disease (McGraw-Hill, New York) and Inborn Errors of Development: The Molecular Basis of Disorders of Morphogenesis (Oxford University Press, San Francisco). He was appointed Assistant Professor of Genetic Medicine in the McKusick Nathans Institute of Genetic Medicine (IGM) in mid-2003. His research program combines the data-intense genomic analyses implemented within the Institute of Genetic Medicine (IGM) with the use of experimental models to facilitate dissection of disease mechanisms and the development of novel, genotype-specific therapeutic strategies.