Peter Baumann is no stranger to reptiles. He and his wife breed lizards, and they’ve managed to get out of a tight spot facing a couple of rattlesnakes during a hiking trip. But for Baumann, reptiles are more than a hobby; they are part of his research. He wants to understand how some lizards thrive and reproduce in the absence of males by a process called parthenogenesis—producing eggs that develop without the aid of sperm—a phenomenon found in a few dozen vertebrate species.

Baumann’s primary research interest, however, focuses on learning how chromosome ends are protected from being mistaken as DNA breaks, which could elicit a DNA damage response that would be lethal to cells. His research could help identify compounds that limit the life span of tumor cells.

During his graduate studies at the United Kingdom’s Imperial Cancer Research Fund (now Cancer Research UK), he probed the molecular machinery that cells use to repair double-strand breaks in DNA—damage that could prove fatal. He was attracted to the problem, in part, by the enthusiasm of his mentor, Stephen West. “Steve brought this field to life for me,” Baumann says. “After listening to Steve for an hour I couldn’t imagine doing my Ph.D. on anything else.” And the timing was right. “Genetics and biochemistry were really starting to come together” to reveal the secrets of DNA repair in complex organisms. Working with West, Baumann was the first to demonstrate that a protein called Rad51 in humans could catalyze the chromosome pairing and strand exchange that allow cells to fix broken DNA without losing the information it contains.

As a postdoctoral fellow, Baumann found himself drawn to the chromosomes’ tips. He was intrigued by a puzzling observation: the same proteins that recognize double-strand DNA breaks and initiate their repair appear to also associate with telomeres, the structures that cap the ends of healthy chromosomes. “How, then, do cells distinguish broken DNA from chromosome ends,” wondered Baumann. To find out, he joined the lab of HHMI investigator Thomas Cech at the University of Colorado at Boulder. There he identified, in human cells and in fission yeast, a telomere-binding protein called POT1, which protects the ends of chromosomes. The work was published in Science in 2001. When the protein is missing in yeast, its chromosomes unravel and fuse into an unmanageable mess.

Baumann also noticed that POT1 regulates the activity of telomerase, the enzyme that maintains the telomeres. Tightly regulating telomerase assembly and activity is key to the health of the organism: in humans, too little telomerase can lead to tissue degeneration; too much can promote cancer.

At the Stowers Institute for Medical Research since 2002, Baumann continues to explore how cells maintain their chromosomes and keep them from fraying or fusing. He isolated the long sought RNA subunit of fission yeast telomerase, the component that provides the template for telomeric DNA synthesis. Getting his hands on that RNA has allowed Baumann to examine how telomerase is assembled and controlled.

And he continues to study parthenogenesis in lizards, a project he says can provide insights into the evolution of reptile species and of meiosis, the process of cell division that produces egg and sperm. “I don’t know whether, in 10 years, any of this will lead to something medically relevant,” says Baumann. “But so many big breakthroughs have come from a fascination with biological phenomena, and not from a direct motivation to cure a specific disease. So I think if you follow your interests, good things will happen.”