Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans-Knoell-Strasse 8, D-07745 Jena, Germany.
Department of Biosynthesis/NMR, Max Planck Institute for Chemical Ecology, Hans-Knoell-Strasse 8, D-07745 Jena, Germany.
Science. 2021 Jan 15;371(6526):255-260. doi: 10.1126/science.abe4713.
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 causes severe autotoxicity symptoms that result from the inhibition of sphingolipid biosynthesis by noncontrolled hydroxylated diterpene derivatives. Moreover, the diterpenes' defensive function is achieved by inhibiting herbivore sphingolipid biosynthesis through postingestive backbone hydroxylation products. Thus, by regulating metabolic modifications, tobacco plants avoid autotoxicity and gain herbivore defense. The postdigestive 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.
许多植物特化代谢物在抵御食草动物方面发挥作用，而阻断其生物合成途径中的特定步骤通常会导致自毒性。然而，其防御和自毒性的分子机制尚不清楚。在这里，我们表明，沉默参与二萜生物合成的两个细胞色素 P450 在野生烟草中会导致严重的自毒性症状，这是由非控制的羟基化二萜衍生物抑制鞘脂生物合成引起的。此外，二萜类化合物的防御功能是通过抑制草食动物鞘脂生物合成来实现的，这是通过在后消化过程中对骨干进行羟基化来实现的。因此，通过调节代谢修饰，烟草植物可以避免自毒性并获得对草食动物的防御。植物与其昆虫食草动物之间发生的后消化二重奏可以反映植物对利用有效化学防御产生的“有毒废物倾倒”问题的解决方案。
