Georgiev Plamen, Toscano Sarah, Nair Amit, Hardie Roger, Raghu Padinjat
The Inositide laboratory, Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom.
J Neurogenet. 2012 Sep;26(3-4):338-47. doi: 10.3109/01677063.2012.725436. Epub 2012 Oct 8.
During sensory transduction, Drosophila photoreceptors experience substantial increases in intracellular Ca(2+) levels (Ca(2+)). Nevertheless in a number of mutants associated with excessive Ca(2+) influx through transient receptor potential (TRP) channels, Drosophila photoreceptors undergo loss of normal cellular structure manifest as a retinal degeneration. However, the molecular mechanisms that underpin this degeneration process remain unclear. The authors previously isolated a mutant, su(40), that is able to suppress the retinal degeneration seen in photoreceptors from loss-of-function alleles of rdgA that are known to have constitutively active TRP channels. Here the authors report the genetic mapping of su(40) as well the isolation of additional alleles of su(40). Studies of su(40) as well as these new alleles should facilitate the understanding of the mechanisms by which excessive Ca(2+) influx results in retinal degeneration.
在感觉转导过程中，果蝇光感受器细胞内的钙离子水平（[Ca(2+)]i）会大幅升高。然而，在一些与通过瞬时受体电位（TRP）通道过度流入钙离子相关的突变体中，果蝇光感受器会出现正常细胞结构丧失，表现为视网膜退化。然而，支撑这种退化过程的分子机制仍不清楚。作者之前分离出了一个突变体su(40)，它能够抑制rdgA功能缺失等位基因的光感受器中出现的视网膜退化，已知这些等位基因具有组成型活性TRP通道。在此，作者报告了su(40)的遗传定位以及su(40)其他等位基因的分离。对su(40)以及这些新等位基因的研究应有助于理解过量钙离子流入导致视网膜退化的机制。
