AND THEN ... VENTER CREATED BACTERIA
J. Craig Venter, the scientist who surreptitiously slipped quite a bit of his own DNA into the human genome project test material, has obtained a $3 million grant from the U.S. Department of Energy to design and create the genes of a new life form using laboratory chemicals. Much of the media coverage of the project has overtones of the 1980 B-grade move, "Attack of the Killer Tomatoes." Venter and colleagues are assuring everyone the new bacteria will not be able to escape or survive outside the lab. Venter said he is trying to solve fossil fuel and environmental problems and address hydrogen as an energy source. "We believe that building a synthetic chromosome is an important step toward realizing these goals because we could potentially engineer an organism with the ideal qualities to begin to cope with our energy issues," he said in a prepared statement issued by his new corporation, the Institute for Biological Energy Alternatives in Rockville, Md. A polio virus has been synthesized from scratch, but this would be the first bacterium to be created.
FLESH-EATING BACTERIAL ACTION LINKED TO GENES
Infections with the flesh-eating bacteria that cause necrotizing fasciitis, a potentially deadly condition, as well as toxic shock are less likely to be severe in people with a particular genetic make-up, report researchers at the University of Tennessee in Memphis. The genes involved, called major histocompatibility complex II, or MHCII, encode highly variable proteins that play a central role in regulating the immune system. "Depending on your MHCII type you can get toxic shock or be protected from it," lead researcher Malak Kotb told UPI's GeneAlert. "A different set of MHCII types were found to predispose or protect certain people from ... necrotizing fasciitis or the flesh-eating syndrome." The researchers said it might be possible to devise therapies and vaccines that take advantage of underlying mechanisms they have discovered. The study is in this week's online issue of Nature Medicine.
TWO GENES CONTROL CHOLESTEROL EXCRETION
Two genes are essential for efficient secretion of cholesterol into the bile, the major route of cholesterol exit from the body, report researchers at the University of Texas Southwestern Medical Center in Dallas. Mice that lacked the two genes and fed a high-cholesterol diet showed liver cholesterol levels 18 times higher and plasma cholesterol levels 2.4 times than mice who had the Abcg5 and Abcg8 genes. High cholesterol levels in the blood are considered a major risk factor for coronary artery heart disease and stroke. "By activating or upregulating Abcg5 and Abcg8 you could theoretically reduce cholesterol in the body by increasing cholesterol transport into the bile and limiting cholesterol absorption. This may also reduce cholesterol in the blood," said Helen Hobbs, senior author of the study. The findings are reported in this week's issue of the Proceedings of the National Academy of Sciences.
GENES LINKED TO SOME SUDDEN INFANT DEATHS
About 5 percent of all cases of sudden infant death syndrome are linked to the babies' genes, report researchers at the sudden death genome laboratory at the Mayo Clinic in Rochester, Minn. The scientists took samples of tissue from 93 babies who had died of SIDS and looked at five genes known to be associated with the electrical impulses that produce a healthy heartbeat pattern. In about 5 percent of the babies who died from SIDS, there were genetic mutations in genes studied that did not occur in DNA samples taken from healthy children. "SIDS will probably turn out to have 20 different underlying causes," said lead researcher author Michael J. Ackerman. "If we can figure out what they are, we can screen for them and hopefully one day, prevent future cases of SIDS." The results were reported this week in Chicago at the American Heart Association's Scientific Sessions 2002.
OBESITY AND DIABETES ASSOCIATED WITH JNK GENE
A high level of activity by a gene called JNK is associated with both obesity and insulin resistance, scientists at the Harvard School of Public Health report. Insulin resistance is a central problem in type 2 diabetes. Obesity is closely associated with insulin resistance and considered the leading risk factor for type 2 diabetes mellitus. The researchers used mice bred with and without the JNK gene. They found JNK mice fed a high-fat diet were more likely to become obese and develop subsequent insulin resistance than those without JNK. "(The gene is) an attractive target for new therapeutic drugs to treat the most prevalent metabolic diseases around the world: obesity, insulin resistance and type 2 diabetes," said researcher Gökhan Hotamisligil. The study appears in the Nov. 21 issue of the British journal Nature.
(EDITORS: For more information on VENTER, contact Heather Kowalski at 301-309-3400 or [email protected]. For FLESH EATERS, Malak Kotb at 901-448-7247 or [email protected]. For CHOLESTEROL, Amy Shields at 214-648-3404 or [email protected]. For SIDS, Carole Bullock at 214-706-1279 or [email protected]. For JNK, Kevin Myron at 617-432-4388 or [email protected])
