Department of Biological Science and Graduate School of Analytical Science and Technology, Chungnam National University, Daejeon, Korea.
Plant Physiol. 2010 Nov;154(3):1514-31. doi: 10.1104/pp.110.161869. Epub 2010 Sep 27.
Anthocyanin accumulation is regulated negatively by ethylene signaling and positively by sugar and light signaling. However, the antagonistic interactions underlying these signalings remain to be elucidated fully. We show that ethylene inhibits anthocyanin accumulation induced by sucrose (Suc) and light by suppressing the expression of transcription factors that positively regulate anthocyanin biosynthesis, including GLABRA3, TRANSPARENT TESTA8, and PRODUCTION OF ANTHOCYANIN PIGMENT1, while stimulating the concomitant expression of the negative R3-MYB regulator MYBL2. Genetic analyses show that the ethylene-mediated suppression of anthocyanin accumulation is dependent upon ethylene signaling components responsible for the triple response. Furthermore, these positive and negative signaling pathways appear to be under photosynthetic control. Suc and light induction of anthocyanin accumulation was almost fully inhibited in wild-type Arabidopsis (Arabidopsis thaliana) ecotype Columbia and ethylene (ethylene response1 [etr1-1]) and light (long hypocotyl1 [hy1], cryptochrome1/2, and hy5) signaling mutants treated with the photosynthetic electron transport inhibitor 3-(3,4-dichlorophenyl)-1,1-dimethylurea. The transcript level of the sugar transporter gene SUC1 was enhanced in ecotype Columbia treated with the ethylene-binding inhibitor silver and in etr1-1, ethylene insensitive2 (ein2-1), and ein3 ein3-like1 mutants. In contrast, 3-(3,4-dichlorophenyl)-1,1-dimethylurea treatment reduced SUC1 expression, which indicates strongly that SUC1 represents an integrator for signals provided by sugar, light, and ethylene. SUC1 mutations lowered accumulations of anthocyanin pigment, soluble sugar content, and ethylene production in response to Suc and light signals. These data demonstrate that the suppression of SUC1 expression by ethylene inhibits Suc-induced anthocyanin accumulation in the presence of light and, hence, fine-tunes anthocyanin homeostasis.
花色素苷的积累受到乙烯信号的负调控和糖和光信号的正调控。然而，这些信号之间的拮抗相互作用仍有待充分阐明。我们表明，乙烯通过抑制正向调节花色素苷生物合成的转录因子的表达，包括 GLABRA3、TRANSPARENT TESTA8 和 PRODUCTION OF ANTHOCYANIN PIGMENT1，从而抑制蔗糖（Suc）和光诱导的花色素苷积累，同时刺激负调节因子 MYBL2 的伴随表达。遗传分析表明，乙烯介导的花色素苷积累抑制依赖于负责三重反应的乙烯信号成分。此外，这些正向和负向信号通路似乎受到光合作用的控制。在野生型拟南芥（Arabidopsis thaliana）哥伦比亚生态型和乙烯（etr1-1）和光（long hypocotyl1 [hy1]、cryptochrome1/2 和 hy5）信号突变体中，Suc 和光诱导的花色素苷积累几乎完全被光合作用电子传递抑制剂 3-(3,4-二氯苯基）-1,1-二甲基脲抑制。在哥伦比亚生态型中，用乙烯结合抑制剂银处理或在 etr1-1、乙烯不敏感 2（ein2-1）和 ein3 ein3-like1 突变体中，糖转运蛋白基因 SUC1 的转录水平增强。相比之下，3-(3,4-二氯苯基）-1,1-二甲基脲处理降低了 SUC1 的表达，这强烈表明 SUC1 是糖、光和乙烯信号的整合因子。SUC1 突变降低了对 Suc 和光信号的花色素苷色素、可溶性糖含量和乙烯产生的积累。这些数据表明，乙烯对 SUC1 表达的抑制抑制了光下 Suc 诱导的花色素苷积累，从而精细调节花色素苷稳态。
