Li et.al_Science_source_data

Many plant specialized metabolites function in herbivore defense and abrogating particular steps in their biosynthetic pathways frequently causes autotoxicity. However, the molecular mechanisms underlying their defense and autotoxicity remain unclear. Here, we show that silencing two cytochrome P450s involved in diterpene biosynthesis in the wild tobacco, Nicotiana attenuata, causes severe autotoxicity symptoms that result from the inhibition of sphingolipid biosynthesis by non-controlled hydroxylated diterpene derivatives. Moreover, the diterpene’s defensive function is achieved by inhibiting herbivore sphingolipid biosynthesis through post-ingestive backbone hydroxylation products. Thus, by regulating metabolic modifications, tobacco plants avoid autotoxicity and gain herbivore defense. The post-digestive duet that occurs between plants and their insect herbivores can reflect the plant’s solutions to the “toxic waste dump” problem of using potent chemical defenses.诸多植物特有代谢物（plant specialized metabolites）在抵御植食性动物的过程中发挥功能，而阻断其生物合成通路中的特定步骤常会引发自毒作用（autotoxicity）。然而，这类代谢物介导防御与产生自毒作用的分子机制仍不明晰。本研究显示，在渐狭烟草（Nicotiana attenuata）中沉默两个参与二萜生物合成（diterpene biosynthesis）的细胞色素P450（cytochrome P450）基因，会引发严重的自毒症状，该症状源于失控的羟化二萜衍生物对鞘脂生物合成（sphingolipid biosynthesis）的抑制。此外，二萜的防御功能可通过摄食后骨架羟化产物，抑制昆虫植食者的鞘脂生物合成来实现。综上，植物通过调控代谢修饰规避自毒作用，并获得抵御植食性动物的能力。植物与其昆虫植食者之间的这种消化后互作体系，可视为植物应对“使用强效化学防御所产生的有毒废物堆积”问题的解决方案。