Recorded: 08 May 2012
Well, working as a PhD student with an electron microscope, we looked at bacteria, we looked at viruses, bacteriophages, and I studied—there were some already available mutants of bacteriophage lambda, and these mutants did not reproduce entirely. But they produced upon induction of their production. They produced sometimes heads, but no tails. Or no DNA filled in in the head, in the particle. So I looked at these structures, and one day I had a mutant, which was received from the Lederbergs, this was transducing phage 4. Bacterial genes for galactose fermentation, and there was nothing to be seen at all. So I felt there may be no genes present for the head and tail formation. So, at that moment I decided to go into genetics, and study genetics, and indeed it turned out that head and tail genes were missing in this phage. So, the conclusion, together with [??] at that moment, was that this was a hybrid, having substituted some of the phage genes by host genes, host genes for galactose fermentation
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.