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Lunch with a Laureate: Robert Horvitz

04/27/2010 12:00 PM Museum
H. Robert Horvitz, '68, David H. Koch Professor of Biology, MIT

Description: As an undergraduate at MIT, Robert Horvitz did not take a biology course until his senior year. But after only six weeks into his first class with professor Cy Leventhal, he realized this was the field for him. He boldly asked for a recommendation as part of his application to grad school-in biology. "Is it too late?" he wanted to know. Professor Leventhal explained that his own undergraduate and graduate degrees had been in physics and that Horvitz would, in fact, be "starting early."

It was his work in Cambridge, England, however, that set the stage for the discoveries for which he would receive the Nobel Prize in 2002. Here he worked with Sidney Brenner and John Sulston on a phenomenon called "programmed cell death" or apoptosis. Cell death occurs naturally as part of the genetic program of every cell-a tadpole loses its tail as it turns into a frog, a bird that doesn't need webbed feet loses the webbing as it develops. But for many years biologists ignored this behavior thinking that they must be doing something wrong when cells they were studying died.

When Horvitz first began work on the analysis of programmed cell death, he didn't study human or animal diseases. Instead, he relied on a tiny nematode-C. elegans-only 1mm in length and comprised of exactly 959 cells. He had been warned that C. elegans was obscure and that using it would be a "scientific dead end." Nonetheless, this creature proved to be the perfect "research subject" for the genetic and molecular work he did in understanding apoptosis. "It's very easy to study an organism . . . that simple."

Today cell death-cellular suicide-is recognized as a normal part of the development and biology of animal cells. Disease, on the other hand, is seen as an abnormality in the regulation of programmed cell death. According to Horvitz, diseases come in "two flavors"-cells in which there is too little programmed cell death (cells that should die, instead live) and cells in which there is too much programmed cell death (cells that should live, instead die).

Horvitz also emphasizes the importance of basic research and the importance of federal funding for that work. "If all funding is targeted to specific areas, then out"of"the"box discoveries wouldn't happen and progress would be much slower."

About the Speaker(s): David H. Koch Professor of Cancer Biology at MIT; Investigator, Howard Hughes Medical Institute H. Robert Horvitz won the 2002 Nobel Prize in Physiology or Medicine (with Sydney Brenner and John Sulston), for his work on programmed cell death (apoptosis), and for his studies concerning organ development in C. elegans. His apoptosis studies may also improve the understanding of neurological disorders such as amyotrophic lateral sclerosis (ALS), a disease that killed Horvitz's father in 1989. In collaboration with others, Horvitz identified a gene involved in the inherited form of ALS, and he is also pursuing other genes involved in the disease. "My hope is that my discoveries will one day lead to advances in medicine that alleviate human suffering and contribute to the world in ways that will benefit mankind," Horvitz has said. He is also an investigator for the Howard Hughes Medical Institute and a member of the McGovern Institute for Brain Research at MIT, and a member of the MIT Center for Cancer Research. He holds appointments at the Massachusetts General Hospital in neurology and in medicine. Horvitz received bachelor's degrees in mathematics and economics from MIT (1968) and an M.A. and Ph.D. (1974) in biology from Harvard University. He was a postdoctoral researcher at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England. He joined the faculty of MIT in 1978 and became professor of biology in 1986 and an investigator of the Howard Hughes Medical Institute in 1988.

Host(s): Office of the Provost, MIT Museum

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