PROTEIN-KINASE-C IS REQUIRED FOR LIGHT ADAPTATION IN DROSOPHILA PHOTORECEPTORS
PROTEIN-KINASE-C IS REQUIRED FOR LIGHT ADAPTATION IN DROSOPHILA PHOTORECEPTORS
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DOI：
10.1038/363634a0
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发表时间：
1993-06-17
期刊：
影响因子：
64.8
通讯作者：
MINKE, B
中科院分区：
文献类型：
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作者：
HARDIE, RC;PERETZ, A;MINKE, B
蛋白激酶 C (PKC) 是许多细胞过程的关键酶1,2，但人们对它的生理作用知之甚少。果蝇 3-5 中眼睛特异性 PKC 和无效 PKC 突变体 inaC(P209) 的鉴定提供了研究 PKC 功能的绝佳机会（参考文献 5,6）。传递到 inaC 光感受器的明亮调节光会导致离解小眼的全细胞记录灵敏度异常丧失；这被解释为“超适应”，并且 PKC 的作用被认为与光适应不同5。一个可能相关的发现是，在强光下，inaC 的响应下降到基线6。无脊椎动物的光感受器使用磷酸肌醇信号级联7-12，通过所谓的量子凸点13响应单光子，这些量子凸点加起来形成对光的宏观响应14-16。光适应允许感光器在巨大的环境强度范围内调整其灵敏度14,17。尽管光适应的分子机制仍不清楚，但它是一种负反馈过程12，由胞质钙的增加12,18和肿块大小的减少12,14-16介导。我们现在表明，在生理条件下，inaC 的光适应能力严重降低，这表明眼睛特异性 PKC（本身由胞质钙 4,5 和二酰甘油的增加激活）是适应所必需的。此外，我们表明，在缺乏 PKC 的情况下，单个肿块无法正常终止，这种效应可以解释 inaC 表型的多效性表现。
PROTEIN kinase C (PKC) is a key enzyme for many cellular processes1,2 but its physiological roles are poorly understood. An excellent opportunity to investigate the function of PKC has been provided by the identification of an eye-specific PKC in Drosophila3-5 and a null PKC mutant, inaC(P209) (refs 5,6). Bright conditioning lights delivered to inaC photoreceptors lead to an abnormal loss of sensitivity in whole cell recordings from dissociated ommatidia; this has been interpreted as 'hyperadaptation' and PKC's role has been suggested to be distinct from light adaptation5. A presumably related finding is that during intense light, the response of inaC declines to baseline6. Invertebrate photoreceptors use the phosphoinositide signalling cascade7-12, responding to single photons with so-called quantum bumps13 which sum to form the macroscopic response to light14-16. Light adaptation allows photoreceptors to adjust their sensitivity over the enormous range of ambient intensities14,17. Although the molecular mechanism of light adaptation remains obscure, it is a negative-feedback process12 mediated by a rise in cytosolic calcium12,18 and a decrease in bump size12,14-16. We now show that under physiological conditions light adaptation is severely reduced in inaC, suggesting that eye-specific PKC, itself activated by a rise in cytosolic calcium4,5 and diacylglycerol, is required for adaptation. Furthermore, we show that in the absence of PKC individual bumps fail to terminate normally, an effect that can account for the pleiotropic manifestations of the inaC phenotype.