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Archive - Oct 7, 2009

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Bacterium May Aid Formation of Gold

Scientists in Australia, together with collaborators, have shown that a particular bacterium (Cupriavidus metallidurans) catalyzes the biomineralization of gold by transforming toxic gold compounds to their metallic form using an active cellular mechanism. “A number of years ago we discovered that the metal-resistant bacterium C. metallidurans occurred on gold grains from two sites in Australia. The sites are 3,500 km apart, in southern New South Wales and northern Queensland, so when we found the same organism on grains from both sites we thought we were onto something. It made us wonder why these organisms live in this particular environment. The results of this study point to their involvement in the active detoxification of Au complexes leading to formation of gold biominerals,” explained Dr. Frank Reith, first author of the research report. The experiments showed that C. metallidurans rapidly accumulates toxic gold complexes from a solution prepared in the lab. This process promotes gold toxicity, which pushes the bacterium to induce oxidative stress and metal resistance clusters, as well as an as yet uncharacterized Au-specific gene cluster in order to defend its cellular integrity. This leads to active biochemically-mediated reduction of gold complexes to nano-particulate, metallic gold, which may contribute to the growth of gold nuggets. This is the first direct evidence that bacteria are actively involved in the cycling of rare and precious metals, such as gold. These results open the doors to the production of biosensors that may help mineral explorers find new gold deposits. This work was published on October 7 in the online edition of PNAS.

Beta Cell Growth, Insulin Production Increased in Diabetic Mice

By “knocking out” the Lkb1 gene in the beta cells of diabetic laboratory mice, scientists have been able to increase the size and number of beta cells and also to increase the amount of insulin stored in and released by these cells. “We were surprised by the impressive accumulation of Lkb1 in beta cells of diabetic mice, which suggested that Lkb1 might contribute to their impaired function. After removal of the Lkb1 gene, the beta cells grow larger, proliferate more, and secrete more insulin. It's a one-stop shop for the much needed insulin", said Dr. Robert Screaton, senior author of the research report. Importantly, the improved beta cell function lasted for at least five months, even in mice fed a high-fat diet designed to mimic the high caloric intake associated with metabolic syndrome and type 2 diabetes in humans. "The knockout mice on a high-fat diet have lower blood glucose. If this observation is confirmed in humans, it may give us another clue into the development of type 2 diabetes, and perhaps new treatment options,” Dr. Screaton said. This work was published in the October 7 issue of Cell Metabolism. [Press release] [Cell Metabolism abstract]