Their study suggests that this degeneration was caused by overactive TRP channels, which allowed calcium ions to accumulate in the cells, thus killing them. In a second group of flies, Pak disrupted the inaF gene so that it could not produce the INAF protein. In addition to not producing the INAF protein, the flies in this group showed a significant reduction in the amount of TRP protein produced and nearly shut down the activities of the TRP channel, Pak says. Though part of the shutdown of the TRP channels may be attributed to a reduction in the amount of the TRP protein available, Pak's group found additional evidence that mutations in the inaF gene also have a direct effect on TRP channel activity. In flies containing mutations in both the inaF gene and the trp gene, the study found that the degenerative effects displayed by fruit flies with a trp mutation are suppressed.
Flies normally have two copies of the trp gene.
Even if only one of these contains the new mutation, the photoreceptors will degenerate completely within two to three days. If inaF mutations are introduced into the same flies, no degeneration is observed for more than two weeks. Pak says the findings suggest that the INAF protein may play a regulatory role in the function of the TRP channel. However, if it turns out to be true, INAF would be the first example of a regulator protein for the TRP-related calcium channels. Because the TRP protein is related to a number of proteins found in humans, the findings may have long-term implications for finding new ways to suppress or control some degenerative diseases.