In the dynamic world of the developing brain, neural stem cells give rise to neurons deep within the brains fluid-filled ventricles. These newborn neurons then migrate along the stem cell fibers up to the neocortex, the seat of higher cognitive functions. Now, scientists have discovered a key mechanism of this migration one that may also play an important role in other developmental processes and diseases, including cancer.
The finding, the cover story in a recent issue of Nature (Aug. 23, 2007), was led by Laura Elias, a neuroscience graduate student in the laboratory of senior author Arnold Kriegstein, MD, PhD, a professor of neurology and director of the UCSF Institute for Regeneration Medicine.
Elias is one of 16 UCSF CIRM Stem Cell Scholars up and coming young scientists funded by the California Institute for Regenerative Medicine, established by California voters in 2004 to allocate $3 billion over 10 years to support stem cell research.
Scientists have known that migration of neurons depends in part on motors within the cells that drive their movement along the neural stem cell fibers. They have also known that this migration depends on receptors on the neurons surface that sense signals in the environment that either repel or attract the cells, thus directing their path.
But little has been known about the molecules that mediate the interaction between the migrating neurons and the neural stem cell fiber itself. And relatively overlooked in this process has been the possible role of so-called gap junctions.
Gap junctions are pores, or channels, that form between cells. They are created when two hemi-channels, each in the membrane of a different cell, connect. The junctions are well known for their role in enabling cells to pass molecular signals to one another. In developing tissue, they are particularly active in supporting signaling that promotes cell proliferation, or cell division.
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| Contact: Jennifer OBrien jobrien@pubaff.ucsf.edu 415-476-2557 University of California - San Francisco Source:Eurekalert |
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