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How cancer cells survive. In mice, the well-studied p53 tumor suppressor gene interacts with two other genes — called PUMA and Noxa — to trigger cell death in response to DNA damage. Researchers in Shai Shaham’s laboratory have now identified the roundworm equivalent of the mouse Noxa gene, which they’ve named ced-13. Their experiments in C. elegans indicate that ced-13 gene expression or activity depends on p53, and that overexpression of ced-13 increases the number of cells that die, providing additional evidence that the p53 pathway is evolutionarily conserved. The finding has implications for understanding how cancer cells survive attempts to destroy them and may aid in the development of better tumor-fighting agents. Shaham is head of the Laboratory of Developmental Genetics.
Cell Death and Differentiation, January 12, 2005

Molecular pinch-hitter. Before potassium ions can enter a cell through a channel in the cell’s membrane, they must be separated from other ions. The cell achieves this by queuing up the potassium ions in a molecular tube formed from four amino acids. This tube, which acts as a filter, has puzzled scientists because it seems to defy nature: its shape requires amino acids that are essentially mirror images of each other — left- and right-handed — but the cell only makes “left-handed” amino acids from which to assemble it. Now Tom Muir and Roderick MacKinnon have shown that the filter works because glycine, one of its amino acids, is ambidextrous. That is, glycine is a surrogate “right-handed” amino acid in the potassium filter. Glycine’s being the only natural amino acid that can play this role helps explain why the potassium ion filters of all organisms are identical. Muir is head of the Selma and Lawrence Ruben Laboratory of Synthetic Protein Chemistry; MacKinnon is head of the Laboratory of Molecular Neurobiology and Biophysics.
Proceedings of the National Academy of Sciences, December 7, 2004

Insulin insight. MicroRNAs, which contain just 21 to 23 segments, jam the cell’s translation of RNA to protein and, in doing so, regulate biological processes. Markus Stoffel, Thomas Tuschl and colleagues at three other institutions recently identified a new microRNA that helps control the secretion of insulin. In studies with mouse cells, they showed that the microRNA called miR-375 is found only in the insulin-producing pancreatic “islet cells” and not in other tissues or organs. When they overexposed the cells to miR-375, insulin secretion was suppressed by about 40 percent; too little miR-375, on the other hand, enhanced secretion. The researchers also discovered the gene miR-375 interferes with — the Myotrophin (Mtpn) gene — and determined that miR-375 acts independently of other factors that affect insulin secretion, such as changes in glucose metabolism. This makes miR-375 a potential target for drugs to treat diabetes. Stoffel is head of the Robert and Harriet Heilbrunn Laboratory of Metabolic Diseases; Tuschl is head of the Laboratory of RNA Molecular Biology.
Nature, November 11, 2004

Drug-defying bugs. New strains of Staphylococcus aureus that are resistant to vancomycin, the antibiotic of last resort in bacterial infections that withstand all other drugs, have raised the spectre of untreatable staphylococcal disease. Research led by Alexander Tomasz sheds new light on the mechanism of vancomycin resistance in staph as a first step toward finding new ways of controlling these dangerous multi-drug resistant pathogens. Vancomycin kills bacteria by trapping the building blocks of the bacterial cell wall and preventing them from reaching sites where these blocks are linked together to surround the bacterium. Resistant bacteria produce wall building blocks of novel chemical structure, which are not recognized and cannot be trapped by the antibiotic. The Rockefeller scientists identified the bacterial protein, penicillin binding protein (PBP) 2, that is primarily responsible for rerouting these new building blocks in resistant cells for the production of a protective cell wall. The study suggests that selective inhibitors of PBP2 should block vancomycin resistance in staphylococci. Tomasz is head of the Laboratory of Microbiology.
Antimicrobial Agents and Chemotherapy, December 2004

January 28, 2005



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