Welcome the New Neighbors


What remains of the child raised on a cattle farm in central Texas are the good manners and an intrinsic curiosity for the natural world around him. From participating in his high school’s Future Farmers of America (FFA) organization to completing graduate studies at the Massachusetts Institute of Technology (MIT), Randal Halfmann, PhD, has immersed himself in the scientific aspects of his experiences. Supported by a FFA scholarship, Halfmann attended Texas A&M and majored in genetics. Encouraged by his mentor at A&M, he applied for a National Science Foundation fellowship and pursued graduate work at MIT.

It was at MIT where he first began to think seriously about studying particles of misfolded proteins, called prions. At the time, prions had a notorious reputation for being the cause of mad cow disease and its human counterpart, Creutzfeldt-Jakob disease. But Halfmann’s research over the next five years produced two notable papers that helped identify at least one positive attribute of these problem proteins.

In a 2009 Cell paper and a 2012 Nature paper, Halfmann and colleagues demonstrated that in some yeast, prionization — a cascading assembly of proteins into aggregates that alter the normal flow of biological information — actually helped yeast adapt to environmental change. This ignited Halfmann’s interest in identifying the adaptive behaviors aggregated proteins might foster.

With this novel idea and support from competitive grants, Halfmann landed a position at The University of Texas Southwestern Medical Center, bypassing traditional postdoctoral training. There, he began a research program that looked at how proteins aggregate together into prion form and how that change is passed from parent yeast to daughter yeast. Additionally, he showed that some prions function as part of immune response in mammalian cells.

Attracted by the generous support provided to investigators, Halfmann joined the Stowers Institute in August and will continue his research of proteins. Halfmann is excited by the promising future he sees at the Institute. “The Institute puts science first and removes obstacles that might keep scientists at other places from doing what they do best,” he says.



While a student at the Max Planck Institute in Germany with Nobel Laureate Christiane Nüsslein-Volhard, Nicolas Rohner, PhD, had no idea that his research on fish genetics would intersect with the medieval history of the region where he grew up.

Scale-less carp is a dietary mainstay of the Franconia area of Germany where Rohner spent his youth. Turns out the findings in a 2009 Current Biology paper authored by Rohner pinpoint the genetic mutation that monks selected for when domesticating the carp in the Middle Ages. Rohner showed that a gene called Fibroblast Growth Factor Receptor 1 is necessary for fish to develop scales, and mutations in this gene lead to the desired phenotype.

Although Rohner’s current line of research investigates why vertebrates, and fish in particular, exhibit diverse genetic traits, his initial foray into science led him down a different path. Rohner earned a bachelor’s degree at Friedrich-Alexander University in Erlangen, Germany, and went on to research antibodies that target leukemia cells while obtaining an MS degree in biology.

By then, Rohner was looking for new challenges and decided to pursue a doctoral degree in developmental biology using zebrafish as a model organism. This research avenue eventually led him to the fish he currently focuses on — the sightless cavefish, Astyanax mexicanus.

Cavefish have adapted to their dark environment and thus, now lack eyes. In addition, the fish may feed only once a year when food is available. Rohner was intrigued by their ability to maintain good health under such adverse conditions. His research, published this year in the Proceedings of the National Academy of Sciences, found that cavefish have a mutation in a gene for a receptor called MC4R, apparently allowing the fish to binge eat to the point of obesity. In normal fish, intact MC4R serves as a satiety signal and even the human counterpart of MC4R is mutated in some forms of inherited obesity.

In his lab at the Stowers Institute, Rohner will continue his studies focused on the genetic basis of adaptation and metabolism. He is energized by the freedom he now has to take risks in research. “I came in with what sounded like a very unusual model system to study obesity,” he explains. “The Institute has provided me the tools to develop it into an important one to help us better understand developmental biology and eventually provide new insights into human health.”