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Aquatic motion detectors. Fish detect the motion of water with a sensory system called the lateral line, a row of clustered sensory receptors known as neuromasts. Each sensory cell is innervated by a nerve fiber that extends from a ganglion located near the ear. Neuromasts form from a stream of cells that migrates along the animal from the ear to the tail. This stream of cells also serves during the organism’s development as a scaffold that guides the migration of the nerve fibers and supporting cells called glia. Studying zebrafish, Hernán López-Schier and A. James Hudspeth have discovered that mutant animals that lack glia develop twice the usual number of neuromasts, suggesting that glia play a role in inhibiting the overproduction of neuromasts. The finding provides insight into the genetic basis for changes in developmental timing — inherited sensory alterations that might allow a fish to colonize new niches, avoid predators, or capture novel prey. Hudspeth is F.M. Kirby Professor and head of the Laboratory of Sensory Neuroscience.

Proceedings of the National Academy of Sciences, February 1, 2005

Old bottle, new vaccine. Just one dose of the vaccine against yellow fever protects against the disease for 30 years or more, a fact that is crucial in tropical Africa and South America, where the virus is endemic and few people have the chance to be vaccinated more than once. Now Charles Rice and colleagues at the NYU School of Medicine have taken an important step toward using the yellow fever vaccine against another tropical disease — malaria. They placed a gene from the malaria parasite into 17D, as the yellow fever vaccine is known, and then injected malaria-infected mice with the hybrid. The single injection greatly reduced the level of malaria parasites in the livers of the mice and conferred lasting resistance against later exposure. The study opens the door to using 17D as the basis for vaccines against many other infections, including AIDS. Rice is Maurice R. and Corinne P. Greenberg Professor and head of the Laboratory of Virology and Infectious Disease.

Journal of Experimental Medicine, January 17, 2005

Changing channels. Two new studies by David Gadsby’s laboratory provide some hints on what does, and does not, regulate the activity of the cystic fibrosis chloride channel (CFTR), which allows salts to move in and out of the body’s cells. By deleting different segments of the protein, Gadsby and colleagues showed that two unique parts of the CFTR that were thought to regulate the channel, first seen in a crystal structure published last year, actually do not. However, when Gadsby and Rockefeller’s Brian Chait examined several of the sites in the CFTR where signal-mediated phosphorylation occurs, they found that one amino acid in particular is important for helping the channel distinguish signals from noise. When this site is phosphorylated — when a phosphate group is attached to it — only a strong stimulus can activate the CFTR. Mutations to the site, meanwhile, cause the channel to become much more sensitive. The CFTR is one member of a family that also includes proteins involved in cancer multi-drug resistance and hypoglycemia, and an understanding of how the CFTR protein works may shed light on how other members of the family function. Gadsby is head of the Laboratory of Cardiac and Membrane Physiology.

Journal of General Physiology, January 2005, February 2005

Short stopper. A recent paper by Titia de Lange and Jacqueline J. L. Jacobs shows that a protein called p16INK4a is important for detecting when strands of DNA called telomeres have become too short. Telomeres act as caps that get shorter with every cell division, as chromosomes lose a small amount of DNA each time a cell replicates. They protect important genetic sequences from getting lost. However, extremely short telomeres can destabilize the structure of a chromosome, making breaks and rearrangements that lead to cancer more likely. de Lange and Jacobs found that p16INK4a can cause a cell to stop growing when it senses very short telomeres. The role of p16INK4a in this process, called telomere-directed senescence, has been controversial, and de Lange and Jacobs hope the new data will aid in the understanding of the genetics behind tumorigenesis. de Lange is Leon Hess Professor and head of the Laboratory of Cell Biology and Genetics.

Current Biology, December 29th, 2004

May 13, 2005



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