When a cell protector collaborates with a killer

New research reveals what it takes for a protein that is best known for protecting cells against death to take on the opposite role.

From early development to old age, cell death is a part of life. Without enough of a critical type of cell death known as apoptosis, animals wind up with too many cells, which can set the stage for cancer or autoimmune disease. But careful control is essential, because when apoptosis eliminates the wrong cells, the effects can be just as dire, helping to drive many kinds of neurodegenerative disease.

By studying the microscopic roundworm Caenorhabditis elegans — which was honored with its fourth Nobel Prize last month — scientists at MIT’s McGovern Institute for Brain Research have begun to unravel a longstanding mystery about the factors that control apoptosis: how a protein capable of preventing programmed cell death can also promote it. Their study, led by Robert Horvitz, the David H. Koch Professor of Biology at MIT, and reported Oct. 9 in the journal Science Advances, sheds light on the process of cell death in both health and disease.

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