Abiotic and biotic factors cause plant wounding and trigger complex short- and long-term responses at the local and systemic levels. These responses are under the control of complex signaling pathways, which are still poorly understood. Here, we show that the rapid activation of clade-A mitogen-activated protein kinases (MAPKs) MPK3 and MPK6 by wounding depends on the upstream MAPK kinases MKK4 and MKK5 but is independent of jasmonic acid (JA) signaling. In addition, this fast module does not control wound-triggered JA accumulation in Arabidopsis (Arabidopsis thaliana), unlike its orthologs in tobacco. We also demonstrate that a second MAPK module, composed of MKK3 and the clade-C MAPKs MPK1/2/7, is activated by wounding in a MKK4/5-independent manner. We provide evidence that the activation of this MKK3-MPK1/2/7 module occurs mainly through wound-induced JA production via the transcriptional regulation of upstream clade-III MAP3Ks, particularly MAP3K14. We show that mkk3 mutant plants are more susceptible to herbivory from larvae of the generalist lepidopteran herbivore Spodoptera littoralis, indicating that the MKK3-MPK1/2/7 module is involved in counteracting insect feeding.

非生物和生物因素导致植物受伤，并在局部和全身水平引发复杂的短期和长期反应。这些响应受复杂的信号通路的控制，人们对此仍然知之甚少。在这里，我们显示通过伤口快速激活进化枝A丝裂原活化蛋白激酶（MAPKs）MPK3和MPK6取决于上游MAPK激酶MKK4和MKK5，但独立于茉莉酸（JA）信号传导。此外，该快速模块无法控制在拟南芥（Arabidopsis thaliana）中伤口触发的JA积累），与烟草中的直系同源物不同。我们还证明了由MKK3和进化枝C MAPKs MPK1 / 2/7组成的第二个MAPK模块通过以MKK4 / 5独立的方式受伤而被激活。我们提供的证据表明，此MKK3-MPK1 / 2/7模块的激活主要通过上游进化枝III MAP3K（尤其是MAP3K14）的转录调控，通过伤口诱导的JA产生而发生。我们显示mkk3突变植物更容易从食虫从通用鳞翅目食草动物斜纹夜蛾幼虫的食草性，表明MKK3-MPK1 / 2/7模块参与抵消昆虫的摄食。