Recorded: 08 May 2012
Actually, I mentioned, well, putting together in the in vitro gene vector together with segments of DNA from any bacterium are the start of genetic engineering. And we discussed, in 1972, in a workshop near Basel, when that was an EMBO workshop on restriction modification systems. I think Hamilton Smith was also there, and other Americans, and in particular some American colleagues said, well, we have to have a debate on risk evaluation. And we did so one full evening, and we said, well, that’s something we have to seriously consider. And that led later on to this letter to Science in ’74 and to the Asilomar Conference in February ’75. And in the Asilomar Conference it wasn’t—kind of general conclusions that we have to consider two types of risks. One type of risk of genetic engineering is that you end up having a toxic gene or a gene making pathogenicity, and you may, as a researcher, infect yourself with that kind of thing. Which should be avoided. And the second would be a longer term risk, thinking that at some later time one wanted to deliberate into free nature the recombinant DNA and at that moment it may spread to other living beings. So, at that moment me and other people realized, I and other people realized, that we should know actually how Darwinian evolution works at the molecular level. That means we have to find out what is the genetic alteration for a genetic variant.
Werner Arber, (born June 3, 1929, Gränichen, Switz.), Swiss microbiologist, corecipient with Daniel Nathans and Hamilton Othanel Smith of the United States of the Nobel Prize for Physiology or Medicine for 1978. All three were cited for their work in molecular genetics, specifically the discovery and application of enzymes that break the giant molecules of deoxyribonucleic acid (DNA) into manageable pieces, small enough to be separated for individual study but large enough to retain bits of the genetic information inherent in the sequence of units that make up the original substance.
Arber studied at the Swiss Federal Institute of Technology in Zürich, the University of Geneva, and the University of Southern California. He served on the faculty at Geneva from 1960 to 1970, when he became professor of microbiology at the University of Basel.
During the late 1950s and early ’60s Arber and several others extended the work of an earlier Nobel laureate, Salvador Luria, who had observed that bacteriophages (viruses that infect bacteria) not only induce hereditary mutations in their bacterial hosts but at the same time undergo hereditary mutations themselves. Arber’s research was concentrated on the action of protective enzymes present in the bacteria, which modify the DNA of the infecting virus—e.g., the restriction enzyme, so-called for its ability to restrict the growth of the bacteriophage by cutting the molecule of its DNA to pieces.