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When poor communication pokes you in the eye
Date:4/7/2008

in the sequence of the gene building blocks can lead to proteins with limited or completely lost functions: and in this way, in the worst case, to serious diseases or development disorders. The Neuherberg eye researchers gave the name Gjf1 to the gene responsible for the alterations of the Aey12 mutant mice. It is a member of the Connexin family. The genes belonging to this group get the information for the construction of channel proteins, which build the cell to cell connections, Graw declares. Such channels are of great importance for the interchange between cells: also, among other things, between the fiber cells of the developing eye lens itself.

The scientists now speculate that through the newly discovered mutation, the structure of the Gjf1 channel protein is changed, and in this way the formation of the channel is hindered. But through this, the communication between the developing lens fibers would break down. Thus, it would be conceivable that signal molecules essential for the development of the lens are no longer exchanged, or only to a limited extent. In this scenario, faulty cell communication would be the cause of the development of the fibers stopping: and ultimately, of the cloudiness of the eye lens, which would otherwise be transparent. This very phenomenon is also observed in cataracts in humans, a common disease, which appears mostly in the elderly: in Germany alone more than half a million operations are carried out annually, in which the cloudy and opaque lens is replaced with an implant. Our results will surely also provide an insight into the origin of cataracts, Graw adds. Moreover, so far, there has not yet been any mutation in humans equivalent to Gjf1 gene of mice. But this will now change soon, for sure.


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Contact: Dr. Jochen Graw
graw@helmholtz-muenchen.de
49-893-187-2610
Helmholtz Zentrum Mnchen - German Research Center for Environmental Health
Source:Eurekalert

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