His research on DNA helped scientists understand the origins of cancer and other diseases.
By Alyssa Botelho April 5 at 10:36 AM Nobel laureate Sydney Brenner, who escaped poverty in his native South Africa to become one of the heroes of molecular biology’s golden age and, with the help of a translucent soil worm, provided vital clues to understanding diseases such as cancer, Alzheimer’s and AIDS, died April 5 in Singapore, where he had a home and helped develop scientific institutes. He was 92.
Nobel laureate Sydney Brenner in 2003. Any conflicts tended to be overshadowed by the major advances Dr. Brenner made in molecular biology. At the Cambridge lab in the late 1960s, he undertook an ambitious search for a model organism to study complex animal development on a genetic level — uncharted territory at the time.
The humble worm’s DNA has turned out to be surprisingly similar to our own, helping us understand how our cells grow uncontrollably to cause cancer, and why they die in excess in neurodegenerative disorders, heart attacks and AIDS. Young Sydney’s first home was in the back of his father’s shoe shop, two rooms he remembered smelling perpetually of leather. The public library became a haven, and it was there he found “The Science of Life,” the book that first turned him on to biology. Too poor to buy his own copy, he reported the book missing to the library instead and accepted a small fine.
With future Nobel laureate François Jacob at the Pasteur Institute and Matthew Meselson at Harvard, Dr. Brenner proved in 1961 the existence of “messenger RNA.” The molecule, they found, is a key intermediary between DNA and protein — a translated version of the genetic code that is sent out to direct synthesis in the cell’s protein-making factories.
Dr. Brenner’s team mapped the entire cellular anatomy of the worm’s brain and spinal cord, from tip to tail. Worms with strange morphologies or behaviors, such as abnormal locomotion or feeding, were of special interest. From these specimens, Dr. Brenner worked backward to figure out which faulty neurons might cause the behavior, and then which genes in those neurons had been mutated.
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