Nakagawa Takao, Vosshall Leslie B
Laboratory of Neurogenetics and Behavior, The Rockefeller University, New York, NY 10065, USA.
Curr Opin Neurobiol. 2009 Jun;19(3):284-92. doi: 10.1016/j.conb.2009.07.015. Epub 2009 Aug 5.
There is broad consensus that olfactory signaling in vertebrates and the nematode C. elegans uses canonical G-protein-coupled receptor transduction pathways. In contrast, mechanisms of insect olfactory signal transduction remain deeply controversial. Genetic disruption of G proteins and chemosensory ion channels in mice and worms leads to profound impairment in olfaction, while similar mutations in the fly show more subtle phenotypes. The literature contains contradictory claims that insect olfaction uses cAMP, cGMP, or IP3 as second messengers; that insect odorant receptors couple to G(alpha)s or G(alpha)q pathways; and that insect odorant receptors are G-protein-coupled receptors or odor-gated ion channels. Here we consider all the evidence and offer a consensus model for a noncanonical mechanism of olfactory signal transduction in insects.
人们普遍认为，脊椎动物和线虫秀丽隐杆线虫中的嗅觉信号传导使用典型的G蛋白偶联受体转导途径。相比之下，昆虫嗅觉信号转导的机制仍存在很大争议。小鼠和蠕虫中G蛋白和化学感应离子通道的基因破坏会导致嗅觉严重受损，而果蝇中的类似突变则表现出更微妙的表型。文献中存在相互矛盾的说法，即昆虫嗅觉使用cAMP、cGMP或IP3作为第二信使；昆虫气味受体与G(α)s或G(α)q途径偶联；以及昆虫气味受体是G蛋白偶联受体或气味门控离子通道。在这里，我们考虑了所有证据，并提出了一种昆虫嗅觉信号转导非典型机制的共识模型。
