I phoned Daphne, my wife and we both said ‘oh my God’,” he said.Sulston, who was knighted in 2001, said he may use his share of the prize money to further his study of alternatives to market-orientated globalisation.He said he was interested in how research and intellectual property are handled. Brenner is now at the Molecular Sciences Institute in Berkeley, California where he is working on the genetics of the puffer fish and the chimpanzee.Sulston, who last year retired as head of the Wellcome Trust Sanger Institute in Cambridge where he led Britain’s efforts on the human genome project, said that the prize came as a surprise.”I just had a phone call from Sweden in the morning I was here in the lab. Horvitz, 55, is now at the Massachusetts Institute of Technology. elegans have counterparts in humans,” the Karolinska Institute said yesterday. We now know that most genes that are involved in controlling cell death in C. I convinced Bob that they were both data, and that my observations were at least as rich in data as his measurements, if not more so,” he said.In a series of scientific publications beginning in 1976 Sulston not only mapped the lineage of every nematode cell, he also described the visible steps in programmed cell death and demonstrated the first genetic mutations involved in the process.Horvitzbuilt on Brenner’s and Sulston’s insights with a series of elegant experiments in which he identified the first two bone fide “death genes”, ced-3 and ced-4, which played a critical role in programmed cell suicide.”Horvitz showed that the human genome contains a ced-3-like gene. Bob Horvitz, originally from Chicago, was a mathematically trained economist with a thirst for hard data.Writing in his book The Common Thread, Sulston remembers Horvitz as “bespectacled, intense and extremely thorough in his approach” and steeped in the hi-tech ambience of the American East Coast laboratories.”When Bob looked at what I had been doing, just looking down a microscope and drawing, he was unimpressed, ‘Where’s the data?’ he asked me,” Sulston said.”He couldn’t understand how you could do any kind of analysis if you didn’t have something like a tape or readings from a scintillation counter ….

“He said I was 20 years ahead of my time,” Brenner said.In 1969, Brenner recruited a young post-doctoral researcher to his nematode team. Jim Watson, the codiscoverer of the DNA double helix, said the project was too ambitious and that he wouldn’t give Brenner a penny to do it. Each mature worm has exactly 959 cells and its rapid development from egg to adult can be easily viewed down a microscope.Many of Brenner’s colleagues were sceptical. elegans was the perfect subject for a study of how a complete organism can be made from the genetic code of DNA.

Hopefully there will be many others,” he added.The Nobel Assembly of the Karolinska Institute in Stockholm said it was awarding the prize for the team’s discoveries concerning the “genetic regulation of organ development and programmed cell death” – or how a many-celled body is sculpted into shape by a trade-off between cell division and cell suicide.Studies of the nematode worm, Caenorhabditis elegans, led to a fundamental reappraisal of the importance of genes in the deliberate killing of certain cells during normal development. The Cold Spring group’s findings will be published next week.. People thought this type of gene was not important but our research is a sign that it may have a role in cancer.”The same research group at Cold Spring Harbour Laboratory, led by Dr Michael Wigler, identified one of the only other tumour suppressor genes – called PTEN – to be clearly associated with sporadic cancer in 1997.The research group at the University of Washington, led by Dr Mary-Claire King, discovered the first gene linked to hereditary breast cancer, BRCA1, in 1990. Studies showed when the active gene was introduced to breast cancer cells it had the power to kill them or stop them growing.Dr Masaaki Hamaguchi, lead researcher, said: “More than half of sporadic breast cancer has some kind of genetic activity that can switch off DBC2, suggesting this gene has an anti-breast cancer effect.”This is a totally new type of gene and its role in the normal cell is not known.