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Archive - May 9, 2013


Study Discovers Organizing Principle of Bacteria in Biofilms

Bacteria on a surface wander around and often organize into highly resilient communities known as biofilms. It turns out that they organize in a rich-get-richer pattern similar to many economies, according to a new study by researchers at UCLA, Northwestern University, and the University of Washington. The study, published online on May 8, 2013 in Nature, is the first to identify the strategy by which bacteria form the micro-colonies that become biofilms, which can cause lethal infections. The research may have significant implications for battling stubborn bacterial infections that do not respond to antibiotics. Bacteria in biofilms behave very differently from free-swimming bacteria. Within biofilms, bacteria change their gene expression patterns and are far more resistant to antibiotics and the body's immune defenses than individual, free-swimming bacteria, because they mass together and are protected by a matrix of proteins, DNA, and long, chain-like sugar molecules called polysaccharides. This makes seemingly routine infections potentially deadly. Dr. Gerard Wong, professor of bioengineering at the UCLA Henry Samueli School of Engineering and Applied Science, member of the California NanoSystems Institute, and professor of chemistry and biochemstry at UCLA; Erik Luijten, professor of materials science and engineering and of applied mathematics at Northwestern University; and Matthew R. Parsek, professor of microbiology at the University of Washington, led a team of researchers that elucidated the early formation of biofilms by developing algorithms that describe the movements of the different strains of the bacterium Pseudomonas aeruginosa and by conducting computer simulations to map the bacteria's movements. P. aeruginosa can cause lethal, difficult-to-treat infections, including those found in cystic fibrosis and AIDS patients.

Sweeping Analysis of the Embryonic Epigenome

A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis online on May 9, 2013 in Cell of how genes are turned on and off to direct early human development. Led by Dr. Bing Ren of the Ludwig Institute for Cancer Research, Dr. Joseph Ecker of The Salk Institute for Biological Studies, and Dr. James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but in that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences. After an egg has been fertilized, it divides repeatedly to give rise to every cell in the human body—from the patrolling immune cell to the pulsing neuron. Each functionally distinct generation of cells subsequently differentiates itself from its predecessors in the developing embryo by expressing only a selection of its full complement of genes, while actively suppressing others. "By applying large-scale genomics technologies," explains Dr. Ren, Ludwig Institute member and a professor in the Department of Cellular and Molecular Medicine at the UC San Diego School of Medicine, "we could explore how genes across the genome are turned on and off as embryonic cells and their descendant lineages choose their fates, determining which parts of the body they would generate." One way cells regulate their genes is by DNA methylation, in which a molecule known as a methyl group is tacked onto cytosine—one of the four DNA bases that write the genetic code.