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Raymond Rodriguez
Director, Center of Excellence in Nutritional Genomics, University of California Davis Davis, CA, USA
Nutritional Genomics
Monday, September 13, 2010
10:30 - 11:00 am

The mechanisms by which nutrient and non-nutrient bioactives influence long-term health outcomes are not well understood. For example, how do low-potency dietary signals regulate thousands of genes in hundreds of pathways to reduce disease risk? Do dietary signals interact with the genome randomly, or are these interactions targeted in a regio-specific fashion? While the genomic revolution has provided an array of powerful analytical tools to investigate human health, many researchers continue to use reductionist approaches to study complex diet-genome interactions. Researchers have focused too intently on isolating individual food bioactive at the expense of discovering novel synergistic effects of combinations of dietary signals. Researchers have also relied too heavily on genetic theories of disease, ignoring important genetic modifiers such as nutrition, lifestyle, exercise and epigenetics — factors that make human health a complex system. As a complex system, human physiology consists of networks genes, proteins and metabolites that are interconnected in interdependent at the boundary between deterministic processes and chaotic (i.e., unpredictable) processes. In response to nutritional stress, adaptive, self-organizing molecular and cellular responses emerge to return the network to homeostasis. Such behaviors are called nutridynamical systems or time-dependent molecular and cellular states that emerge in response to small changes in nutritional input. For one type of nutritional input, self-organizing, adaptive behaviors can emerge that return the network to homeostasis while other kinds of inputs can produce chaotic behaviors can prolong the return to homeostasis. The latter may increase the chances that a chaotic, or disease state, will emerge. The difficulty in integrating dietary signaling with current genetic control and signal sensing mechanisms is the lack of regulatory models that incorporate diet-influenced phase transitions and other non-linear effects. Diet-informed epigenetic modifications of chromatin could represent a new regulatory motif with the potential to produce large changes in gene expression in response to low-potency dietary signals.
Dr. Rodriguez is a professor in the Department of Molecular & Cellular Biology in the College of Biological Sciences at the University of California, Davis. After receiving his Ph.D. at the University of California, Santa Cruz in 1974, he was an A.P. Giannini Foundation Fellow in the laboratory of Herbert W. Boyer at UC San Francisco Medical Center where he helped develop many of the molecular cloning technologies that now serve as the foundation of the modern biotechnology industry. Dr. Rodriguez joined the faculty at the UC Davis in 1977 and is actively involved in research and teaching at the undergraduate and graduate level. Dr. Rodriguez has been actively involved in all aspects of biotechnology as well as and holds 17 patents. In 2003 he became director of the Center of Excellence for Nutritional Genomics, a multi-investigator, multi-institutional research program to study the impact of diet-genome interactions on human health. He has published numerous articles and books on molecular biology and biotechnology and is currently working on a new book entitled, Dietary Regulation of Gene Expression and its Impact on Human Health. His current research focus is nutritional epigenomics or the study of how plant-based dietary factors alter human gene activity by chromatin modification.

Click to view Raymond Rodriguez's ABIC 2010 presentation