Common mechanisms regulating dark noise and quantum bump amplification in Drosophila photoreceptors
Common mechanisms regulating dark noise and quantum bump amplification in Drosophila photoreceptors
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DOI：
10.1152/jn.00001.2013
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发表时间：
2013-04-01
影响因子：
2.5
通讯作者：
Hardie, Roger C.
中科院分区：
文献类型：
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作者：
Chu, Brian;Liu, Che-Hsiung;Hardie, Roger C.
朱波，刘超，Sengupta S, Gupta A, Raghu P, Hardie RC。果蝇光感受器中调节暗噪声和量子碰撞放大的共同机制。中国生物医学工程学报（英文版），2009,31(4):444 - 444。首次发表于2013年1月30日；doi: 10.1152 / jn.00001.2013。绝对视觉阈值受到“暗噪声”的限制，在果蝇的光感受器中，“暗噪声”主要是由短暂的（类似于10毫秒）、小的（类似于2 pA）内向电流事件主导，发生速度类似于2/s，据信反映了自发的G蛋白激活。肌球蛋白III （NINAC）的点突变破坏了其与支架蛋白INAD的相互作用，从而增加了这些暗事件的速率和幅度。这种表型模拟了先前描述的ninaC零突变（无失活，无后电位；编码肌球蛋白III）和相关蛋白亲视网膜蛋白（rtp）。在二酰基甘油激酶（rdgA/+）的杂合子突变体中，暗噪声也同样增加。在ninaC、rtp和rdgA/+突变体中，G(q) α亚基（G α q）和主要光敏通道（trp）的突变极大地抑制了暗噪声，但视紫红质却没有。ninaC、rtp和rdgA/+突变也都促进了G α q和PLC亚形态的残留光响应。在亚微摩尔范围内提高细胞质Ca2+增加暗噪声，促进外源性激动剂激活瞬时受体电位（TRP）通道，并再次促进G α q次形态的光响应。我们的研究结果表明，RTP、NINAC、INAD和二酰基甘油激酶，以及Ca2+依赖性阈值，在抑制暗噪声和调节量子碰撞产生中具有共同的作用；因此，大多数自发G蛋白激活在正常条件下不能产生暗事件。相比之下，量子肿块的产生是可靠的，但延迟到足够的G蛋白和PLC被激活以克服阈值，从而确保产生具有高量子效率的全尺寸肿块。
Chu B, Liu CH, Sengupta S, Gupta A, Raghu P, Hardie RC. Common mechanisms regulating dark noise and quantum bump amplification in Drosophila photoreceptors. J Neurophysiol 109: 2044-2055, 2013. First published January 30, 2013; doi:10.1152/jn.00001.2013.-Absolute visual thresholds are limited by "dark noise," which in Drosophila photoreceptors is dominated by brief (similar to 10 ms), small (similar to 2 pA) inward current events, occurring at similar to 2/s, believed to reflect spontaneous G protein activations. These dark events were increased in rate and amplitude by a point mutation in myosin III (NINAC), which disrupts its interaction with the scaffolding protein, INAD. This phenotype mimics that previously described in null mutants of ninaC (no inactivation no afterpotential; encoding myosin III) and an associated protein, retinophilin (rtp). Dark noise was similarly increased in heterozygote mutants of diacylglycerol kinase (rdgA/+). Dark noise in ninaC, rtp, and rdgA/+ mutants was greatly suppressed by mutations of the G(q) alpha-subunit (G alpha q) and the major light-sensitive channel (trp) but not rhodopsin. ninaC, rtp, and rdgA/+ mutations also all facilitated residual light responses in G alpha q and PLC hypomorphs. Raising cytosolic Ca2+ in the submicromolar range increased dark noise, facilitated activation of transient receptor potential (TRP) channels by exogenous agonist, and again facilitated light responses in G alpha q hypomorphs. Our results indicate that RTP, NINAC, INAD, and diacylglycerol kinase, together with a Ca2+-dependent threshold, share common roles in suppressing dark noise and regulating quantum bump generation; consequently, most spontaneous G protein activations fail to generate dark events under normal conditions. By contrast, quantum bump generation is reliable but delayed until sufficient G proteins and PLC are activated to overcome threshold, thereby ensuring generation of full-size bumps with high quantum efficiency.