Shoji Tsubasa, Hashimoto Takashi
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0101, Japan.
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0101, Japan.
Phytochemistry. 2015 May;113:41-9. doi: 10.1016/j.phytochem.2014.05.017. Epub 2014 Jun 16.
Plants have evolved diverse defense metabolites as adaptations to biotic and abiotic stresses. The defense alkaloid nicotine is produced in Nicotiana tabacum (tobacco) and its biosynthesis is elicited by jasmonates in the roots. At least seven jasmonate-responsive genes that encode transcription factors of the Ethylene Response Factor (ERF) family are clustered at the nicotine-regulatory locus NICOTINE2 (NIC2) in the tobacco genome. A subset of the NIC2-locus ERFs and their homologs, including ERF189 and ERF199, have been shown to be most effective in controlling nicotine biosynthetic pathway genes. Herein reported is that the ERF genes of this group, other than ERF189 and ERF199, were strongly induced by NaCl in tobacco hairy roots, although salt stress had no effect on expression of nicotine biosynthesis genes. Abscisic acid and osmotic stress also increased expression of a subset of these NaCl-inducible ERF genes. Promoter expression analysis in transgenic tobacco hairy roots confirmed that while methyl jasmonate (MJ) activated the promoters of ERF29, ERF210 and ERF199, salt stress up-regulated the promoters of only ERF29 and ERF210, but not ERF199. The protein biosynthesis inhibitor cycloheximide induced expression of the ERFs, and simultaneous addition of MJ and cycloheximide showed synergistic effects. These results indicate that, after several gene duplication events, the NIC2-locus ERFs and possibly their homologs appear to have diverged in their responses to jasmonates and various environmental inputs, including salt stress, and may have evolved to regulate distinct metabolic processes and cellular responses.
植物已经进化出多种防御性代谢产物以适应生物和非生物胁迫。防御性生物碱尼古丁在烟草中产生，其生物合成由根部的茉莉酸酯引发。在烟草基因组中，至少有七个编码乙烯反应因子（ERF）家族转录因子的茉莉酸酯响应基因聚集在尼古丁调控位点NICOTINE2（NIC2）处。NIC2位点的一部分ERF及其同源物，包括ERF189和ERF199，已被证明在控制尼古丁生物合成途径基因方面最为有效。本文报道，除ERF189和ERF199外，该组ERF基因在烟草毛状根中受到NaCl的强烈诱导，尽管盐胁迫对尼古丁生物合成基因的表达没有影响。脱落酸和渗透胁迫也增加了这些NaCl诱导型ERF基因的一部分的表达。转基因烟草毛状根中的启动子表达分析证实，虽然茉莉酸甲酯（MJ）激活了ERF29、ERF210和ERF199的启动子，但盐胁迫仅上调了ERF29和ERF210的启动子，而没有上调ERF199的启动子。蛋白质生物合成抑制剂环己酰亚胺诱导了ERF的表达，同时添加MJ和环己酰亚胺显示出协同效应。这些结果表明，在几次基因复制事件之后，NIC2位点的ERF及其可能的同源物在对茉莉酸酯和各种环境输入（包括盐胁迫）的反应中似乎已经发生了分化，并且可能已经进化到调节不同的代谢过程和细胞反应。
