Li C, Geng C, Leung H T, Hong Y S, Strong L L, Schneuwly S, Pak W L
Department of Biological Sciences, 1392 Lilly Hall, Purdue University, West Lafayette, IN 47907-1392, USA.
Proc Natl Acad Sci U S A. 1999 Nov 9;96(23):13474-9. doi: 10.1073/pnas.96.23.13474.
The trp gene of Drosophila encodes a subunit of a class of Ca(2+)-selective light-activated channels that carry the bulk of the phototransduction current. Transient receptor potential (TRP) homologs have been identified throughout animal phylogeny. In vertebrates, TRP-related channels have been suggested to mediate "store-operated Ca(2+) entry," which is important in Ca(2+) homeostasis in a wide variety of cell types. However, the mechanisms of activation and regulation of the TRP channel are not known. Here, we report on the Drosophila inaF gene, which encodes a highly eye-enriched protein, INAF, that appears to be required for TRP channel function. A null mutation in this gene significantly reduces the amount of the TRP protein and, in addition, specifically affects the TRP channel function so as to nearly shut down its activity. The inaF mutation also dramatically suppresses the severe degeneration caused by a constitutively active mutation in the trp gene. Although the reduction in the amount of the TRP protein may contribute to these phenotypes, several lines of evidence support the view that inaF mutations also more directly affect the TRP channel function, suggesting that the INAF protein may have a regulatory role in the channel function.
果蝇的trp基因编码一类Ca(2+)选择性光激活通道的一个亚基，这类通道承载着大部分光转导电流。在整个动物系统发育过程中都已鉴定出瞬时受体电位（TRP）同源物。在脊椎动物中，已有人提出TRP相关通道介导“储存-操作性Ca(2+)内流”，这在多种细胞类型的Ca(2+)稳态中很重要。然而，TRP通道的激活和调节机制尚不清楚。在此，我们报道果蝇的inaF基因，它编码一种在眼中高度富集的蛋白INAF，该蛋白似乎是TRP通道功能所必需的。该基因的无效突变显著减少了TRP蛋白的量，此外，还特异性地影响TRP通道功能，几乎使其活性丧失。inaF突变还显著抑制了由trp基因的组成型激活突变所导致的严重退化。虽然TRP蛋白量的减少可能导致这些表型，但几条证据支持inaF突变也更直接地影响TRP通道功能的观点，这表明INAF蛋白可能在通道功能中具有调节作用。
