Romero L C, Lam E
AgBiotech Center and Department of Biochemistry and Microbiology, Waksman Institute, Rutgers State University, Piscataway, NJ 08854, USA.
Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1465-9. doi: 10.1073/pnas.90.4.1465.
The transmission process of light signals from plant photoreceptors to target cellular events is largely unknown. In the present work, we show that treatment of dark-adapted soybean cells (SB-P) with cholera toxin or pertussis toxin uncouples phytochrome-dependent gene expression. Addition of as little as 10 ng of toxin per ml is sufficient to activate expression of genes encoding the major chlorophyll a/b-binding protein (cab) in the dark. Significant levels of cab transcript accumulation are detected within 0.5 h after addition of the toxins and expression of these genes is desensitized to further light treatments. Treatment of SB-P cells with the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphtha-lenesulfonamide hydrochloride (W-7) prevents induction of the photoregulated gene by phytochrome or bacterial toxins. These results indicate the involvement of guanine nucleotide binding protein(s) in phytochrome-mediated cab gene activation. A likely site of action for this step is between the photoreceptor and a downstream W-7-sensitive effector.
光信号从植物光感受器到目标细胞事件的传递过程在很大程度上尚不清楚。在本研究中,我们发现用霍乱毒素或百日咳毒素处理暗适应的大豆细胞(SB-P)会使依赖光敏色素的基因表达解偶联。每毫升加入低至10纳克的毒素就足以在黑暗中激活编码主要叶绿素a/b结合蛋白(cab)的基因的表达。在加入毒素后0.5小时内就可检测到显著水平的cab转录本积累,并且这些基因的表达对进一步的光照处理不敏感。用钙调蛋白拮抗剂N-(6-氨基己基)-5-氯-1-萘磺酰胺盐酸盐(W-7)处理SB-P细胞可阻止光敏色素或细菌毒素对光调节基因的诱导。这些结果表明鸟嘌呤核苷酸结合蛋白参与了光敏色素介导的cab基因激活。这一步骤可能的作用位点在光感受器和下游对W-7敏感的效应器之间。