Subject: Scientists Find `Switch' to Halt Bacteria Growth Date: Published: 10/19/90 (82 lines) Source: Wall Street Journal. Copyright Dow Jones & Co. Inc. Technology: Scientists Find `Switch' to Halt Bacteria Growth ---- By Marilyn Chase Staff Reporter of The Wall Street Journal STANFORD, Calif. -- A team of Stanford University scientists has solved one of biology's most basic puzzles, identifying the "off switch" that stops bacteria from replicating. The discovery sheds light on the basic processes of growth. Experts said yesterday it could illuminate new paths in cancer and AIDS research, as well as in the manufacture of biotechnology products. Working with E. coli, a common bacterium, the team discovered a protein that halts replication of the bacterial DNA, the organism's genetic code, and in turn stops cells from dividing. This off switch, called the 33kdA protein, performs a crucial step without which cells grow wildly and out of control, as they do in cancer. The finding comes from the laboratory of Arthur Kornberg, a Stanford biochemistry professor and a past Nobel prize winner for his earlier studies on the replication of DNA. The lead author of the report is Deog Su Hwang, a postdoctoral fellow in the Kornberg lab. Their report is published in the October issue of the journal Cell. "Clearly, this is a major new finding about the biochemistry of DNA replication by Dr. Kornberg, the founding father of the whole field," said John Minna, a researcher at the National Cancer Institute. There are many diseases in which a cell's ability to control DNA replication is impaired, he said, and thus the discovery of such a regulator switch is "very exciting." "It could have profound implications for cancer and AIDS," Mr. Minna said. Dr. Kornberg, who worked on the project for nine years, emphasized that the discovery remains a basic research tool for now -- but one which opens a window on a much larger picture. "If you know the anatomy of the switch," Dr. Kornberg said, "if you have the hood off and can see how the motor works, you can then determine what factors provoke it to get started replicating or keep it in check." "One obvious question," said NCI's Mr. Minna, "is whether there exists a similar protein in human cells. If so, does it act as a tumor-suppressor gene, to hold DNA replication in check? " Future experiments in larger animals and in humans must answer that question. Dr. Kornberg, who was out of the country and unavailable for comment, asserted in a prepared statement that it is "almost inevitable" that the new finding will guide research on human growth. Elliott Crooke, a fellow in the Kornberg laboratory, explained in an interview yesterday that so many bacterial proteins have human counterparts that "we feel confident {it} could very well carry through to these higher organisms." He predicted that scientists will be able to "exploit the negative effect" of the protein in antibiotic development, as well as in cancer treatment, where doctors strive to arrest runaway growth. On the other hand, neutralizing the off switch may become a goal for biotech firms, which harness these common bacteria as tiny factories for churning out biotechnology products. Inactivating that switch, he speculated, could potentially boost the production of gene-spliced proteins. These include such products as human growth hormone or the heart attack drug TPA. "We can hypothesize about how it will carry through, but we set out to find a basic tool, and Deog Su Hwang found it," said Mr. Crooke. "Every time we find one of these factors, it's another piece of the jigsaw puzzle." [This article is made available here by Dow Jones Co. for the personal and non-commercial use of callers to this bbs, in the hope that it will be of some help to those who are suffering from the disease and others who are seeking to help them.]