Thomas Werner

Scientific Background

Dr. Werner became interested in the question “What is life?” as a four-year old child in his parent’s garden in former East Germany. With the age of 10, he began to develop a life-long interest in the biology of butterflies and moths. He has been breeding and collecting them ever since. For his Master’s thesis, he decided to shift his focus to molecular biology because this was a newly emerging field of biology that promised new jobs.

Thus, Dr. Thomas Werner studied the human heart disease-causing virus Coxsackie B3 at the molecular level at Friedrich-Schiller-University Jena in Germany. After the fall of the Berlin Wall, Dr. Werner made one of his childhood dreams become true and moved to Sweden. He spent seven years in Umeå, working on his Ph.D. thesis about the innate immune response in the fruit fly Drosophila melanogaster.

During this time at Umeå University in Dr. Dan Hultmark’s lab, he discovered and described a new family of immune genes that we humans share with flies and many other animals. In 2005, Dr. Werner shifted his research focus towards evolution of development (evo-devo) and worked as a postdoctoral fellow at the University of Wisconsin-Madison in Dr. Sean B. Carroll’s lab, where he established the fruit fly Drosophila guttifera as a new transgenic model organism to investigate how complex animal color patterns evolve.

Current Research Project 1: The evolution and development of complex animal color patterns in Drosophila

Animal color patterns such as zebra stripes, leopard spots, and the myriad variants of butterfly wing color patterns are known to play important ecological and physiological roles in the life of animals and are crucial for the survival of species. Scientists first tried to solve the secret of animal color patterns with mathematical approaches to find models that could explain how these patterns developed. In 1952, Turing, the inventor of the computer, proposed the famous reaction-diffusion model in which a short-range acting activator molecule diffuses from a source to stimulate color production, while a long-range acting inhibitor molecule prevents pigmentation. Using the spectacularly ornamented fruit fly Drosophila guttifera, we identified that the Wingless morphogen had evolved a new function in this species by activating the yellow gene, causing many black melanin spots to appear on the wings. Humans also have the wingless gene, which is a known proto-oncogene (called Wnt-1). Wnt-1 is overexpressed in many tumors, which causes the tumors to proliferate.  We are currently investigating if the color patterns on the abdomen and thorax of Drosophila guttifera are generated by the same pathway as on the wing, or if other proto-oncogenes have evolved a link to pigmentation. Elucidating the pigmentation pathways in this fruit fly can help us understand how cancer-inducing pathways are regulated and how they have evolved.

Current Research Project 2: The evolution of mushroom poison (alpha-amanitin) resistance in Drosophila

Just one Death Cap or Destroying Angel mushroom contains enough toxin to kill a person. Alpha-amanitin is the principal toxin in these deadly-poisonous mushrooms. However, poisonous mushrooms generally contain a mixture of different toxins that target various tissues. Because alpha-amanitin targets the RNA-polymerase II and renders it non-functional, almost all eukaryotic organisms are very sensitive to this toxin. Only a handful of organisms on the planet can eat these mushrooms and survive without harm. Some Drosophila species belong to the resistant organisms. Interestingly, their RNA-polymerase II is highly sensitive to the toxin. Thus, there must be detoxification and/or excretion mechanisms that allow these flies to consume these mushrooms, so that the toxins don’t get to their targets. Being able to eat poisonous mushrooms both provides a unique niche in the eco-system and also kills parasites that would otherwise render the flies sterile. The main goal of Dr. Werner’s research is to elucidate the molecular-genetic mechanisms that cause alpha-amanitin resistance in Drosophila.