Despite the apparent contradiction, cell suicide is an integral part of life itself. A cell's ability to instruct itself to die, a process called apoptosis, is necessary for normal embryonic development of many organisms. For example, apoptosis allows tadpoles to transform into frogs and prunes extra skin so that human fingers and toes are separated, not webbed.

Research by Xiaodong Wang has helped piece together the molecular puzzle of how cells commit suicide. His studies may eventually lead to new treatments for cancer, neurological disorders, and other diseases. Indeed, the malfunction of cell-death genes is a hallmark of many diseases. Cancer and autoimmune diseases can sometimes occur when cells fail to commit suicide. Conversely, neurological disorders and paralysis due to disease or trauma can cause too many cells to die.

Wang's studies have unveiled key biochemical steps in the process of apoptosis in mammalian cells. He has shown that mitochondria play a surprising role in the death process by releasing the mitochondrial proteins cytochrome c, Smac, and endonuclease G. Cytochrome c and Smac activate a cascade of signals that ultimately trigger cell death; endonuclease G causes DNA damage by cleaving chromatin DNA, an event that also leads to apoptosis.

"We now have a good idea of what signals are involved in programmed cell death," Wang said. "What we don't yet know is how these signals are linked to the mitochondria. That connection is an important one in deciding whether cells live or die, and once we figure it out, it could be a target of future therapies."

Wang said his work requires constant interactions with the postdoctoral fellows and graduate students who work in his lab. "The most enjoyable part of my work has been the process of discovery—the enlightening moments of understanding something that was previously unknown," he added.