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Robert C Dickson, PhD




  • Professor

College Unit(s)

Biography and Education


B.S. University of Redlands Ph.D. University of California, Los Angeles


Some people grow old yet show few signs of aging, while others show signs of aging long before they grow old.  How can this be?  We are trying to identify and understand the signal transduction pathways and cellular processes that control the rate of biological aging and lifespan.  Our goal is to develop a way to lower the frequency, slow the progression or delay the onset of age-related diseases including cancer, neurodegeneration, arthritis, cardiovascular pathology and diabetes that diminish health in the elderly and cause the majority of human deaths.

More than eighty years ago researchers found that feeding rats 30-40% fewer calories significantly improved health and increased lifespan.  These results were utterly surprising were mostly ignored for fifty years.  However, over the past twenty-five years, studies using model organisms have reinforced the notion that nutrient restriction, implemented either by reducing total calories (caloric restriction) or total protein/amino acid intake (protein or amino acid restriction), improves health and increases lifespan.  Small-scale studies in humans are beginning to show that nutrient restriction slows aging and promotes a younger more youthful physiological state.  But more research is required to fully evaluate the anti-aging effects of nutrient restriction and determine if it ameliorates the aging process and improves health in the elderly.  

The chief drawback of nutrient restriction results from the natural, evolved-desire of humans to eat.  Consequently, most people are not capable of restricting food intake sufficiently and over a long enough period of time to realize the potential health benefits.  Thus, there is an urgent need to develop alternatives because the rapid, worldwide increase in the elderly population is creating medical, social and economic stresses that need to be solved.

We use the common baker’s yeast Saccharomyces cerevisiae as a model eukaryote for studying lifespan because it’s lifespan is short and be analyzed by genetic and biochemical techniques.  Furthermore, many genes involved in regulating lifespan were identified in this organism and it continues to yield new insights into the molecular mechanisms of aging and longevity.   A surprising outcome of studies in model organisms is that similar processes and signaling pathways regulate lifespan in yeasts, worms, flies, and mice.  Humans have many of these processes and signaling pathways, thus, there is a good reason to believe that studies with model organisms will produce alternative ways to mimic nutrient restriction and reduce the burdens presented by aging populations.

We have found that lowering the rate of sphingolipid synthesis in yeasts increases lifespan and does so by regulating processes and signaling pathways that overlap with those that are controlled by nutrient restriction (Adjacent figure - Huang et al., PLoS Genetics, 2012; Liu et al., Aging Cell, 2013).  For our experiments, we use a drug (myriocin) to slow the rate of sphingolipid synthesis.  Besides the results shown in the adjacent figure, we have recently found that myriocin is producing a unique form of protein restriction.  Future research will seek to identify how the drug mimics the effects of protein restriction and enhance longevity.



Diagram summarizing the effects of myriocin treatment on gene transcription in log phase yeast cells during a chronological lifespan (CLS) assay.  The signaling cascades influenced by myriocin treatment include Snf1 (homolog of mammalian AMPK), protein kinase A (PKA), target of rapamycin complex I (TORC1, homolog of mammalian TORC1), Sch9 (homolog of mammalian S6k1/2) and Pkh1/2 (homolog of mammalian PDK1).  Information of Transcription Factors (TFs) can be found at SGD the Saccharomyces Genome Database (

Selected Publications

Research Gate Pubmed Publications