Recorded: 08 May 2012
One problem, which is a partial answer to your question, is that I became more and more aware that nature is very inventive and if you have studied a particular mechanistic process, for example, restriction in E. coli, E. coli K12 bacteria. You cannot extrapolate that all of the restriction systems work in the same way. In fact, the work which was done by Hamilton Smith, originally with hermafluous influenza, also had a restriction system, but the function of this system worked differently. Actually, we do know that the restriction systems which Hamilton Smith studied originally recognized the DNA as foreign, at very short, specific nucleotide sequences, cut it there right away. Our system, which is called type one, while Hamilton Smith has type two enzymes, type one also recognizes non-methylated DNA sequences, specific ones. Each enzyme system has its own recognition sequence, but it does not cut there. It starts to translocate the DNA on both sides, and since there are more restriction recognition sequences on longer DNA molecules, you may start to translocate from another side and when the two translocating enzyme complexes meet each other, it stops, and cuts there. So, it cuts more or less randomly. That’s evolutionary more intelligent than the type two, because the type two will always cut, and if that recognition sequence is an important gene, you cannot acquire so easily that gene. So, but, you know, that shows, and there are many more examples, nature is very inventive. If you have studied one particular mechanism, don’t believe that all these similar processes work precisely in the same way.
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.