Department of Economic Plants and Biotechnology, Yunnan Key Laboratory for Wild Plant Resources, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China.
Tobacco Breeding and Biotechnology Research Center, Yunnan Academy of Tobacco Agricultural Sciences, Key Laboratory of Tobacco Biotechnological Breeding, National Tobacco Genetic Engineering Research Center, Kunming 650021, China.
Plant Sci. 2020 Nov;300:110627. doi: 10.1016/j.plantsci.2020.110627. Epub 2020 Aug 16.
The trade-off between plant growth and resistance to herbivory is thought to be at least partly mediated by the interactions between jasmonates and gibberellins (GAs). Insect herbivory activates jasmonate biosynthesis and signaling, and plant growth is concomitantly inhibited. Whether or not the herbivory-induced jasmonates suppress the accumulation of GAs and thus reduce plant growth, and which jasmonates are functional in this process, remain unclear. In this study, we show that herbivory-induced stunted growth of Nicotiana attenuata was completely dependent on allene oxide cyclase (AOC) and coronatine insensitive1 (COI1), which encode a JA biosynthetic enzyme and the receptor, respectively, but only partially dependent on jasmonic acid-isoleucine conjugate (JA-Ile), the bioactive jasmonate. Quantification of GAs and exogenous treatments indicated that herbivory-induced growth inhibition was caused by GA deficiency, and that the reduction in GA accumulation was strongly associated with both decreased concentrations of GA biosynthetic gene transcripts and transcriptional activation of GA catabolic genes. We further show that JA-Ile only positively regulated the levels of GA catabolic genes, while the accumulation of GA biosynthetic gene transcripts was controlled by certain AOC-derived jasmonate(s) rather than by JA-Ile. This work sheds light on the mechanisms by which plants adapt to herbivory by using intricate phytohormone signaling and transcriptional regulatory networks.
植物生长和抗草食性之间的权衡被认为至少部分受到茉莉酸（jasmonates）和赤霉素（gibberellins，GAs）之间相互作用的调节。昆虫草食性会激活茉莉酸的生物合成和信号传递，同时植物生长受到抑制。食草诱导的茉莉酸是否抑制赤霉素的积累从而减少植物生长，以及哪些茉莉酸在这个过程中起作用，目前仍不清楚。在本研究中，我们表明，烟草原生种（Nicotiana attenuata）受草食性诱导的生长迟缓完全依赖于 1-氨基环丙烷-1-羧酸合酶（allene oxide cyclase，AOC）和冠瘿碱不敏感 1（coronatine insensitive1，COI1），它们分别编码一个 JA 生物合成酶和受体，但仅部分依赖于茉莉酸异亮氨酸（jasmonic acid-isoleucine conjugate，JA-Ile），这是一种有生物活性的茉莉酸。赤霉素的定量和外源处理表明，草食性诱导的生长抑制是由于赤霉素缺乏引起的，而赤霉素积累的减少与 GA 生物合成基因转录物浓度的降低以及 GA 分解代谢基因的转录激活密切相关。我们进一步表明，JA-Ile 仅正向调节 GA 分解代谢基因的水平，而 GA 生物合成基因转录物的积累则由特定的 AOC 衍生的茉莉酸（s）而不是 JA-Ile 控制。这项工作揭示了植物通过利用复杂的植物激素信号和转录调控网络来适应草食性的机制。
