Department of Horticulture, Zhejiang University, Zijingang Campus, 866 Yuhangtang Road, Hangzhou, 310058, China.
School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, B15 2TT, UK.
New Phytol. 2022 Dec;236(5):1796-1808. doi: 10.1111/nph.18455. Epub 2022 Sep 28.
Herbivory severely affects plant growth, posing a threat to crop production. Calcium ion (Ca ) signaling and accumulation of jasmonates (JAs) are activated in plant response to herbivore attack, leading to the expression of defense pathways. However, little is known about how the Ca signal modulates JA biosynthesis. We used diverse techniques, including CRISPR/Cas9, UPLC-MS/MS and molecular biology methods to explore the role of ETHYLENE RESPONSE FACTOR 16 in Ca signal-triggered JA burst during herbivore defense in tomato. Here we show that simulated herbivory induces GLUTAMATE RECEPTOR LIKE3.3/3.5 (GLR3.3/3.5)-dependent increases in electrical activity, Ca influx and increases the abundance of CALMODULIN2 (CaM2) and ERF16 transcripts in tomato. The interaction between CaM2 and ERF16 promotes JA biosynthesis by enhancing the transcriptional activity of ERF16, which increases the activation of ERF16 expression and causes expression of LIPOXYGENASE D (LOXD), AOC and 12-OXO-PHYTODIENOIC ACID REDUCTASE 3 (OPR3), the key genes in JA biosynthesis. Mutation of CaM2 results in decreased JA accumulation, together with the expression of JA biosynthesis-related genes, leading to reduced resistance to the cotton bollworm Helicoverpa armigera. These findings reveal a molecular mechanism underpinning the Ca signal-initiated systemic JA burst and emphasize the pivotal role of Ca signal/ERF16 crosstalk in herbivore defense.
食草动物严重影响植物生长，对作物生产构成威胁。钙离子（Ca ）信号和茉莉酸（JAs）的积累在植物对食草动物攻击的反应中被激活，导致防御途径的表达。然而，人们对 Ca 信号如何调节 JA 生物合成知之甚少。我们使用了多种技术，包括 CRISPR/Cas9、UPLC-MS/MS 和分子生物学方法，来探索乙烯反应因子 16 在番茄食草动物防御中 Ca 信号触发 JA 爆发中的作用。在这里，我们表明模拟的食草动物诱导 GLUTAMATE RECEPTOR LIKE3.3/3.5（GLR3.3/3.5）依赖性的电活性增加、Ca 内流增加以及钙调素 2（CaM2）和 ERF16 转录本的丰度增加。CaM2 和 ERF16 之间的相互作用通过增强 ERF16 的转录活性来促进 JA 生物合成，从而增加 ERF16 表达的激活，并导致脂氧合酶 D（LOXD）、AOC 和 12-氧代-植物二烯酸还原酶 3（OPR3）的表达，这些是 JA 生物合成的关键基因。CaM2 的突变导致 JA 积累减少，同时与 JA 生物合成相关基因的表达减少，导致对棉铃虫 Helicoverpa armigera 的抗性降低。这些发现揭示了 Ca 信号引发系统性 JA 爆发的分子机制，并强调了 Ca 信号/ERF16 串扰在食草动物防御中的关键作用。
