图1. 营养与乙烯信号协同调节植物生长的机制
在营养丰富或未进行乙烯处理时, 蛋白激酶CTR1和TOR均能直接与EIN2发生相互作用, 分别对多个氨基酸进行磷酸化修饰。当采用乙烯处理时, 受体失活, CTR1被抑制, EIN2第645和924位丝氨酸(S645和S924)磷酸化水平下调, 导致EIN2的C端被切割, 一部分入核, 另一部分在细胞质中促进P-body的形成, 最终稳定转录因子EIN3/EIL1, 激活下游基因表达(Li et al. 2015; Hao et al. 2017)。当营养缺乏时, TOR受到抑制, EIN2第657位苏氨酸(T657)磷酸化水平下降, 导致EIN2全长蛋白进入细胞核。如果发生在黑暗中, 会造成EIN3/EIL1蛋白水平上调, 激活下游ERF基因表达, 抑制下胚轴伸长; 如果发生在光下, 会造成E2Fa基因下调, 最终抑制根分生组织细胞的增殖。实线代表已建立直接互作, 虚线代表可能间接互作或尚待研究, 箭头代表促进作用, T型箭头代表抑制作用。

Figure 1. The mechanism of coordinated regulation of plant growth by nutrition and ethylene signaling
Protein kinases CTR1 and TOR can interact and phosphorylate EIN2, respectively, in nutrition-rich medium or ethylene- free environment. When treated with ethylene, inactivation of the receptors leads to the suppression of CTR1 and the phosphorylation levels at two serine residues (S645 and S924) of EIN2 are decreased. EIN2 is therefore cleaved and the C terminus translocates into the nucleus and/or forms P-body in the cytoplasm. Consequently, the master transcription factors EIN3/EIL1 are stabilized and the downstream gene expression is activated (Li et al. 2015; Hao et al. 2017). When nutrition deficiency occurs, TOR is inhibited and the phosphorylation level of a threonine (T657) of EIN2 is decreased, followed by the nuclear shuttling of the full-length EIN2 protein. If it occurs in darkness, EIN3/EIL1 proteins would be promoted, thus to activate the expression of downstream ERF genes and to inhibit hypocotyl elongation. Alternatively, if in light, E2Fa gene expression would be down- regulated, thus to inhibit root meristem cell proliferation. Unbroken lines indicate established interactions, broken lines indicate indirect or hypothetical interactions, arrows indicate stimulatory interactions, bar-headed lines indicate inhibitory interactions.