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Proteins that stitch skin. The skin epidermis acts as Saran Wrap for the body, sealing microbes out and body fluids in. Now, new research from Elaine Fuchs’ Laboratory of Mammalian Cell Biology and Development sheds light on how the individual cells in this flexible wrapper adhere to one another.
To form a sheet of skin, epithelial cells make so-called adherens junctions at the points of stable cell-cell contact. At these junctions, the cells assemble linear cables of actin polymers, which are zipped together with the help of a protein called alpha-catenin. The new research, led by postdoc Agnieszka Kobielak, shows that a protein called formin-1 binds to alpha-catenin to initiate the assembly of actin cables. In cells that lack alpha-catenin, the researchers found that a hybrid protein — composed mostly of formin-1 with only a small amount of alpha-catenin — rescues their ability to make contacts.
Fuchs’s findings, which show that formin-1 can regulate actin polymerization, raise the interesting possibility that actin polymerization may also be required for limb development, a process in which formin-1 is also known to play a role. Fuchs is the university’s Rebecca C. Lancefield Professor and investigator at the Howard Hughes Medical Institute.
Nature Cell Biology, January 2004

New ideas about MS. People with multiple sclerosis have severe problems with nerve signaling because they are missing myelin, an insulating material that normally forms a sheath around nerves. Mice manipulated to have an MS-like disease typically die a few weeks after birth because myelin breaks down within their brains and spinal cords, causing paralysis.
In a recent study, Sidney Strickland, head of the Laboratory of Neurobiology and Genetics, and colleagues found that MS mice with lower levels of fibrin, a blood clotting factor, fare much better. When MS mice were mated with mice lacking a gene for making fibrin, the offspring showed less myelin degradation and less inflammation around their nerves. They also lived longer and developed symptoms of MS later. Mice treated with a fibrin-depleting drug derived from snake venom also showed improvement: demyelination was greatly reduced compared to untreated MS mice.
These results suggest that fibrin could potentially be a target for treating MS and are consistent with the Strickland lab’s earlier studies showing that fibrin interferes with new myelin formation during regeneration of peripheral nerves.
Proceedings of the National Academy of Sciences, April 2004

Cracking the neuron code. Like a telegraph that transmits the dots and dashes of Morse code, the body’s neurons transmit pulsed electrical signals with distinctive rhythms. Scientists have long suspected that the frequency and rhythm of this neuron firing translates into meaningful messages within the brain, but so far the meaning has remained a mystery. Recently, George Reeke, head of the Laboratory of Biological Modelling, and research associate Allan Coop devised a new method for analyzing patterns of neuron firing.
Unlike previous methods, which divide a neuron’s recorded activity into regular, clock-like intervals in which each neuron either did or did not fire, Reeke and Coop’s new method is based on the measured times between firings. Information statistics are calculated from a theoretical distribution that is fit to these data. This has several advantages: it eliminates the need to impose a clock on the firing record, it greatly reduces the amount of data otherwise required, and it gives more accurate results for neurons firing in a regular pattern.
Neural Computation, May 2004

How stress rewires the brain. Studies in rats, carried out in Bruce McEwen’s Laboratory of Neuroendocrinology, have found that high levels of stress may cause atrophy to certain neurons in an area of the brain called the medial prefrontal cortex, a section that in humans is often implicated in post-traumatic stress disorder. The cells, known as apical dendrites, became 20 percent shorter and had 17 percent fewer branches after the rats were subjected to stressful conditions for a 21-day period (see images, below).
The scientists suggest that such cellular changes may impair the ability of the medial prefrontal cortex to respond to hormones released in stressful situations. Further studies with this experimental model may yield clues to the structural basis for post-traumatic stress disorder in humans.
The research was done in collaboration with colleagues at Mount Sinai School of Medicine and the National Institutes of Mental Health Center for Fear and Anxiety. McEwen is the university’s Alfred E. Mirsky Professor.
Neuroscience, March 2004

May 14, 2004



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