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Balancing brain chemistry. Scientists in Paul Greengard’s laboratory have discovered a protein that plays a central role in integrating several major molecular signaling pathways in the brain’s striatum, a region that controls movement and balance. Disruption of these pathways is associated with several diseases of the nervous system, including Huntington’s and Parkinson’s. The new protein, called regulator of calcium signaling (RCS), binds to another protein known as calmodulin, thereby inhibiting its activity. Calmodulin mediates the actions of calcium within cells, which are essential for cell signaling. The researchers found that, through its interaction with calmodulin, RCS mediates the balance between the neurotransmitters acetylcholine and dopamine. The finding opens the door to new therapies. Greengard is the university’s Vincent Astor Professor and head of the Laboratory of Molecular and Cellular Neuroscience.
Science, October 23, 2004

Fluid dynamics. The human respiratory tract is lined with cells that have cilia — tiny hair-like projections that sweep mucus up and out of the lungs. People with a genetic mutation that cripples these cilia cannot clear the mucus and suffer chronic infections. They also sometimes develop hydrocephalus, an accumulation of fluid in the brain. New research from Rockefeller’s Nathaniel Heintz, Ines Ibanez-Tallon, with assistance from the Bio-Imaging Resource Center directed by Alison North, and German colleagues, explains the connection. In experiments with mice, they showed for the first time that, as in the respiratory system, there are cilia-studded cells that line the walls of fluid-filled cavities in the brain called ventricles and push fluid along in the proper direction. A mutation in the mouse gene Mdnah5, analogous to the human counterpart, cripples cilia in these brain cells as well as in respiratory cells. As a result, these mice develop hydrocephalus. Heintz is head of the Laboratory of Molecular Biology.
Human Molecular Genetics, September 15, 2004

Chromosomal end game. Mammalian chromosomes end in long stretches of repeated DNA sequences known as telomeres. These telomeres, in turn, terminate in loops that protect the DNA from damage. Now scientists in Titia de Lange’s laboratory have found that telomeres can be shortened dramatically and quickly by losing loop-sized stretches of DNA in a process called homologous recombination. The culprit is a mutant form of the TRF2 protein. In its normal form, TRF2 protects telomere loops, but a mutant called TRF2deltaB, in combination with other proteins, induces the large DNA deletions. The researchers propose that losing loops may be a normal part of the way cells regulate telomere length, one that could be harnessed in the treatment of certain cancers. de Lange is Leon Hess Professor and head of the Laboratory of Cell Biology and Genetics.
Cell, October 29, 2004

November 19, 2004



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