Sirexnoctilio侵染后,松树的防御相关代谢组特征在很大程度上是未知的,尽管,在大多数情况下,树木被淹没。使用基于LC-MS的非靶向代谢组学,我们揭示了这种昆虫在14岁的辐射松树中引起的系统性代谢变化,全球受影响最大的物种。感染后,针中表达了立即的代谢组改变,包括黄酮醇的上调,黄烷-3-醇,oxyneolignans,生长素,脯氨酸,和色氨酸,在其他人中。黄烷-3-醇(儿茶素和原花青素B1)提出了一种快速诱导的光保护机制,该机制通过将脯氨酸转移为呼吸的替代底物来补偿使光系统降解的进行性萎黄病。同时,谷胱甘肽,谷氨酸,针头中的抗坏血酸水平显著下降,这可能表明树木自侵扰开始以来必须面对的严重氧化应激。它们在长期侵扰后没有得到充分补充,氧化还原稳态可能没有实现,损害树木的生存。然而,在整个侵染过程中,在针叶中检测到的大量生长素过表达可能反映了对木蜂毒液引起的过早衰老的耐受性。相比之下,木材组织的代谢组最初保持不变,尽管它似乎在三个月后崩溃了。总的来说,这项工作中采用的代谢组学策略证明了其在揭示植物化学防御与特定应激源相互作用的基本作用方面的有用性。
Defense-related metabolome traits in pine species after infestation by Sirex noctilio are largely unknown, despite, in most cases, trees being overwhelmed. Using LC-MS-based untargeted metabolomics, we revealed the systemic metabolic changes induced by this insect in 14-year-old Pinus radiata trees, the most affected species worldwide. An immediate metabolome alteration was expressed in needles after infestation, including the up-regulation of flavonols, flavan-3-ols, oxyneolignans, auxins, proline, and tryptophan, among others. The flavan-3-ols (catechin and procyanidin B1) suggested a rapidly induced photoprotection mechanism aided by diverting proline as an alternative substrate for respiration to compensate for the progressive chlorosis that degrades photosystems. Meanwhile, glutathione, glutamate, and ascorbate levels significantly dropped in needles, which may indicate the critical oxidative stress that trees had to face since the onset of the infestation. They were not fully replenished after long-term infestation, and redox homeostasis was probably not achieved, compromising tree survival. Nevertheless, a huge auxins overexpression detected in needles throughout the infestation may reflect tolerance against the premature senescence caused by the woodwasp venom. In contrast, the metabolome of wood tissues remained initially unchanged, although it seems to collapse after three months. Overall, the metabolomics strategy adopted in this work evidenced its usefulness in uncovering the fundamental roles of plants\' chemical defense that govern interactions with specific stressors.