Open AccessINAF, a protein required for transient receptor potential Ca 2+ channel function
Author(s) -
Chenjian Li,
Chaoxian Geng,
Hung-Tat Leung,
Young Seok Hong,
Lydia L. R. Strong,
Stephan Schneuwly,
William L. Pak
Publication year - 1999
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.96.23.13474
Subject(s) - transient receptor potential channel , mutation , biology , microbiology and biotechnology , visual phototransduction , gene , biophysics , protein subunit , mutant , retinal degeneration , genetics , receptor , retina , neuroscience
Thetrp gene ofDrosophila encodes a subunit of a class of Ca2+ -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 Ca2+ entry,” which is important in Ca2+ 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 theDrosophila 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. TheinaF mutation also dramatically suppresses the severe degeneration caused by a constitutively active mutation in thetrp gene. Although the reduction in the amount of the TRP protein may contribute to these phenotypes, several lines of evidence support the view thatinaF mutations also more directly affect the TRP channel function, suggesting that the INAF protein may have a regulatory role in the channel function.