This is an article that relates bacterial communication and virulence factor production with bacterial polyphosphate. Stanford researchers through bacteria identification have found that the polyphosphate inside cells may be involved in determining how dangerous bacteria harm plants, humans and other animals. Polyphosphate is a chain like molecule found in every living cell. In animals, one of it is a phosphate storage reservoir for the production of ATP, which provides the energy to power a cell. In bacteria identification, there are bacteria in polyphosphate that helps these single celled microscopic organisms adapt to nutritional deficiencies, environmental stresses, and even helps them survive the bacterias stationary phase of growth.
Arthur Kornberg in 1990, a Nobel laureate and emeritus professor of biochemistry, and a postdoctoral fellow in his lab, defined the enzyme that produces polyphosphate in E coli bacterium. According to him the enzyme polyphosphate kinase or PPK makes polyphosphate by stringing together many phosphate residues. Members of Kornbergs lab have learned that the PPK enzyme is similar in many bacteria, including several types that cause disease in humans. Organisms such as yeast, plants, humans and other animals have a different kind of enzyme for producing polyphosphate.
Kornberg and his team studied the PPK gene by making mutant strains of bacteria lacking the gene for PPK. Through bacteria identification it was found out that Pseudomonas aeruginosa was used in the study. This bacterium is known to cause dangerous infections in people with a deficient immune system. Without the PPK gene, the bacteria were unable to use their flagella to swim and they were unable to use tiny cell extensions for movement. The team also has found that P. aeruginosa bacteria without the gene are also unable to form microbial communities called biofilms making the bacteria unable to communicate with each other via a process called quorum sensing. Production of the proteins and toxins known as virulence factors, which enable bacteria to cause disease in their host, are also decreased without the presence of the PPK gene. Kornbergs study opens up the possibility of using PPK as a novel antibiotic. Inhibitors of this enzyme could be used as an antibiotic to disrupt cell to xcell communication in bacteria. As of the present, Stanford is already negotiating with pharmaceutical companies to search for potential drugs. READ ARTICLE



May 13th, 2010 at 8:18 am
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