Molecular basis of amplification in Drosophila phototransduction:: Roles for G protein, phospholipase C, and diacylglycerol kinase
Molecular basis of amplification in Drosophila phototransduction:: Roles for G protein, phospholipase C, and diacylglycerol kinase
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DOI：
10.1016/s0896-6273(02)01048-6
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发表时间：
2002-11-14
期刊：
影响因子：
16.2
通讯作者：
Raghu, P
中科院分区：
文献类型：
--
作者：
Hardie, RC;Martin, F;Raghu, P
在果蝇的光感受器中，由于单个视紫红质分子的光异构化，负责产生量子突起的扩增被认为是在磷脂酶C （PLC）的下游介导的，因为据报道，在G蛋白或PLC水平大大降低的突变体中，突起的振幅不受影响。我们现在发现，这种突变体中的量子突起减少了3- 5倍，但通过编码二酰基甘油激酶（DGK）的rdgA基因突变和消耗细胞内ATP，量子突起恢复到接近野生型的值。结果表明，扩增需要激活多个G蛋白和PLC分子，确定DGK是调节扩增的关键酶，并暗示二酰基甘油是果蝇光转导的兴奋信使。
In Drosophila photoreceptors, the amplification responsible for generating quantum bumps in response to photoisomerization of single rhodopsin molecules has been thought to be mediated downstream of phospholipase C (PLC), since bump amplitudes were reportedly unaffected in mutants with greatly reduced levels of either G protein or PLC. We now find that quantum bumps in such mutants are reduced similar to3- to 5-fold but are restored to near wild-type values by mutations in the rdgA gene encoding diacylglycerol kinase (DGK) and also by depleting intracellular ATP. The results demonstrate that amplification requires activation of multiple G protein and PLC molecules, identify DGK as a key enzyme regulating amplification, and implicate diacylglycerol as a messenger of excitation in Drosophila phototransduction.