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SCIENCE BRIEFS
BY BETSY HANSON & KRISTINE KELLY
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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