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Unrestrained retina too much of a good thing

La Jolla, Calif. When primitive nerve cells begin forming an eye in the mouse embryo, they are programmed to build a retina. But the ability to see depends upon connecting the retina to the brain via the optic nerve. Unless these embryonic cells are given the right cue at the right time, they mistakenly form a huge eye that consists entirely of retina and lacks the optic nerve.

The discovery that the retina is the 'default' setting for development in the embryonic eye comes from research by neurobiologist Greg Lemke and his colleagues at the Salk Institute for Biological Studies, published in the current issue of Genes & Development. The scientists carried out their work on the laboratory mouse as a model of human biology.

"Our results suggest that the retina is effectively the default pathway for eye development in mammals," said Lemke. The Salk team showed that two chemical cues, or signalling proteins, must be present in the right place at the right time to shut down this default pathway and allow the optic nerve to develop.

The painstaking work of the Salk team has important consequences since controlling the fate of stem cells implanted into the brain is crucial if these cells are to be safely and effectively used in human therapy.

"This study gives us a fascinating insight into how the parts of the brain are laid out because it is likely that the same model applies throughout the nervous system," said Lemke. "There are likely to be other brain areas whose development relies on blocking a tendency to turn into the same cell types as their neighbor."

Lemke and co-authors Stina H. Mui, Jin Woo Kim and Stefano Bertuzzi studied eye development in genetically engineered mouse embryos that lacked the two signalling proteins Vax1 and Vax2. The mice developed normally until approximately 10 days after conception, at which point they started to develop one large, folded sheet of retina, instead of a retina and an optic nerve.
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Contact: Cathy Yarbrough
yarbrough@salk.edu
858-453-8051
Salk Institute
17-May-2005


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