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The major focus of Dr. Tumer’s laboratory is to understand the ribosome interactions and the mechanism of toxicity of ribosome inactivating proteins (RIPs) and trichothecene mycotoxins.
Ricin is a plant toxin used in targeted killing of cancer cells and is a concern for bioterrorism. The related Shiga toxins (Stxs) produced by Shigella and E. coli O157:H7 (STEC) cause food-borne outbreaks and are major concerns for public health. Currently, there are no vaccines or therapeutics to protect against ricin or STEC. Dr. Tumer’s research played a central role in defining the cellular targets of RIPs and trichothecene mycotoxins. Their studies established a new paradigm for the mechanism of depurination of the sarcin/ricin loop and identified toxin/ribosome interactions as a new target for inhibitor discovery. Dr. Tumer’s lab developed fragment-based lead discovery (FBLD) using surface plasmon resonance (SPR) to discover small molecule inhibitors of ricin and Stxs.
Dr. Tumer studies the mode of action of trichothecene mycotoxins produced by Fusarium graminearum, which causes Fusarium head blight (FHB), a devastating disease affecting cereal crops. There is no effective resistance to FHB in cereals. Using chemical genomics approaches they identified mitochondria as a target of trichothecene mycotoxins and showed that trichothecene-induced oxidative stress plays a major role in trichothecene toxicity. They screened activation tagged Arabidopsis lines for resistance to trichothecenes and identified a novel lipid transfer protein (LTP) that confers resistance to trichothecenes and FHB in wheat.
