关于肌醇磷酸代谢在粗糙脉孢菌生物钟振荡器和蓝光信号转导途径中直接作用的反对证据。
Evidence against a direct role for inositol phosphate metabolism in the circadian oscillator and the blue-light signal transduction pathway in Neurospora crassa.
作者信息
Lakin-Thomas P L
机构信息
Department of Plant Sciences, University of Cambridge, U.K.
出版信息
Biochem J. 1993 Jun 15;292 ( Pt 3)(Pt 3):813-8. doi: 10.1042/bj2920813.
The inositol-depletion hypothesis proposes that the effects of Li+ on cellular functions are the result of inhibition by Li+ of the inositol monophosphate phosphatase and subsequent depletion of inositol lipids. This mechanism has been proposed to account for the effects of Li+ on the period of the circadian oscillator. Inositol phosphate metabolism has also been proposed as part of the blue-light signal-transduction pathway through which the phase of the circadian oscillator can be reset by light pulses. Four predictions of these two hypotheses have been tested in the fungus Neurospora crassa and all have been found to fail: (1) inositol supplementation does not reverse the effects of Li+ on the period of the circadian rhythm; (2) inositol depletion of an inositol-requiring mutant does not mimic the effects of Li+; (3) depletion of inositol lipids does not inhibit the response to light; and (4) a phase-resetting pulse of light does not increase the levels of inositol phosphates, including Ins(1,4,5)P3.
肌醇耗竭假说提出，Li⁺对细胞功能的影响是Li⁺抑制肌醇单磷酸磷酸酶并随后导致肌醇脂质耗竭的结果。有人提出这一机制可解释Li⁺对昼夜节律振荡器周期的影响。肌醇磷酸代谢也被认为是蓝光信号转导途径的一部分，通过该途径，昼夜节律振荡器的相位可被光脉冲重置。这两个假说的四个预测已在真菌粗糙脉孢菌中进行了测试，结果均未得到证实：（1）补充肌醇并不能逆转Li⁺对昼夜节律周期的影响；（2）对需要肌醇的突变体进行肌醇耗竭处理并不能模拟Li⁺的作用；（3）肌醇脂质的耗竭不会抑制对光的反应；（4）光的相位重置脉冲不会增加包括Ins(1,4,5)P3在内的肌醇磷酸水平。
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