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A tale of cell fates
During brain development, cells destined to end up in the central nervous system first have to make a choice-whether to become a neuron or instead a glial cell. Stiles and colleagues at Harvard have now identified a key molecular player in this decision process (Nature Neuroscience, Vol. 4, No. 9, Sep 01). Previous evidence suggested that the expression of a transcription factor called Oligo 1 might promote the development of a particular type of glial cell called an oligodendrocyte. (Transcription factors are molecules that can turn particular genes on or off.) Oligodendrocytes have an important function in the brain, as they form the myelin sheath that envelops the axons of neurons and thus speeds the transmission of neural signals. In the new study, Stiles and colleagues used a sophisticated molecular tool (viral vectors) to introduce Oligo 1 into cortical progenitor cells of the developing mouse central nervous system. When the authors then counted cell types in the forebrain about ten days later, they observed that those cells that were infected with the vector containing Oligo 1 became exclusively glia, and a high percentage of those were oligodendrocytes. Cells injected with a control vector were mainly neurons and astrocytes (another type of glial cell). Further analysis suggested that the reduced number of neurons observed as a result of ectopic expression of Oligo 1 was likely due to reduced neuronal survival (as opposed to reduced formation of neurons). Interestingly, the Down syndrome phenotype results in part from age-related neuronal degeneration, and other studies have shown that the human OLIG genes maps to a region of chromosome 21 that is associated with severe mental retardation in Down patients. Although there are many other genes in this region of the chromosome, it seems plausible that an additional chromosome 21 (as seen in Downs syndrome) could lead to overexpression of OLIG genes, and thus contribute to the neuronal degeneration in Downs syndrome. Contacts: Dr. Charles D. Stiles
Harvard Medical School
Department of Cancer Biology
Dana Farber Cancer Institute
44 Binney Street
Boston, Massachusetts 02115
USA
tel: +1 617 632 3512
fax: +1 617 632 4663
e-mail: charles_stiles@dfci.harvard.edu Dr. Constance L. Cepko
Harvard Medical School
Department of Genetics and Howard Hughes Medical Institute
200 Longwood Ave.
Boston, Massachusetts 02115
USA
tel: +1 617-432-7618
fax: +1 617-432-7595
e-mail: cepko@rascal.med.harvard.edu (C) Nature Neuroscience press release.
Message posted by: Trevor M. D'Souza
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