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Gene controls neural stem cell growth

Researchers have discovered that a gene previously implicated in a variety of forms of cancer is also a key regulator of neural stem cell proliferation. Understanding how the gene, called PTEN, promotes the proliferation of neural stem cells could aid efforts to use stem cells in treating neurological disorders.

Howard Hughes Medical Institute investigator Hong Wu and colleagues at the UCLA School of Medicine reported on the regulatory role of Pten in the November 1, 2001, Science Express, the online counterpart of the journal Science.

According to Wu, PTEN is the second most frequently deleted tumor suppressor gene, giving rise to human cancers including brain, breast, prostate, and endometrial cancers.

There was also evidence, said Wu, that the PTEN protein produced by the gene played a normal role in neural development. It was known that humans who have inherited deletions or mutations of the PTEN gene often showed macrocephaly, or abnormally large brains, she said.

The gene is expressed in the central nervous systems of developing human and mouse embryos, but no one had ever done a detailed study to understand the precise role of PTEN in the nervous system.

Knocking out the gene in mice caused early death in embryos, before significant brain development. So, Wu and her colleagues used the Cre-loxP system to genetically manipulate the mice so that the gene would be knocked out later in gestation. The researchers discovered that knocking out Pten in the mouse embryos appeared to hyper-activate a signaling pathway that regulates cell proliferation and cell death in the brain.

Anatomical studies revealed a significant increase in brain size in the mutant animals. The researchers also noted an increase in the size of the brain cells themselves the first evidence that the PTEN protein regulates cell size in mammals, said Wu. The scientists next used antibodies to mark specific types of brain cells.


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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
1-Nov-2001


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