Wang Jun-Xia, Han Wen-Hao, Xie Rui, Zhang Feng-Bin, Ge Zhi-Wei, Ji Shun-Xia, Liu Shu-Sheng, Wang Xiao-Wei
State Key Laboratory of Rice Biology and Breeding, Ministry of Agriculture Key Lab of Molecular Biology of Crop Pathogens and Insects, Key Laboratory of Biology of Crop Pathogens and Insects of Zhejiang Province, Institute of Insect Sciences, Zhejiang University, Hangzhou, China.
Analysis Center of Agrobiology and Environmental Sciences, Zhejiang University, Hangzhou, China.
Plant Cell Environ. 2025 Jan;48(1):387-405. doi: 10.1111/pce.15135. Epub 2024 Sep 11.
Nicotiana benthamiana, a widely acknowledged laboratory model plant for molecular studies, exhibits lethality to certain insect pests and can serve as a dead-end trap plant for pest control in the field. However, the underlying mechanism of N. benthamiana's resistance against insects remains unknown. Here, we elucidate that the lethal effect of N. benthamiana on the whitefly Bemisia tabaci arises from the toxic glandular trichome exudates. By comparing the metabolite profiles of trichome exudates, we found that 51 metabolites, including five O-acyl sugars (O-AS) with medium-chain acyl moieties, were highly accumulated in N. benthamiana. Silencing of two O-AS biosynthesis genes, branched-chain keto acid dehydrogenase (BCKD) and Isopropyl malate synthase-C (IPMS-C), significantly reduced the O-AS levels in N. benthamiana and its resistance against whiteflies. Additionally, we demonstrated that the higher expression levels of BCKD and IPMS-C in the trichomes of N. benthamiana contribute to O-AS synthesis and consequently enhance whitefly resistance. Furthermore, overexpression of NbBCKD and NbIPMS-C genes in the cultivated tobacco Nicotiana tabacum enhanced its resistance to whiteflies. Our study revealed the metabolic and molecular mechanisms underlying the lethal effect of N. benthamiana on whiteflies and presents a promising avenue for improving whitefly resistance.
本氏烟草是一种广泛认可的用于分子研究的实验室模式植物，对某些害虫具有致死性，可作为田间害虫防治的终结诱捕植物。然而，本氏烟草抗虫的潜在机制尚不清楚。在此，我们阐明本氏烟草对烟粉虱的致死作用源于有毒的腺毛分泌物。通过比较毛状体分泌物的代谢物谱，我们发现51种代谢物，包括5种具有中链酰基部分的O-酰基糖（O-AS），在本氏烟草中高度积累。两个O-AS生物合成基因，支链酮酸脱氢酶（BCKD）和异丙基苹果酸合酶-C（IPMS-C）的沉默，显著降低了本氏烟草中的O-AS水平及其对烟粉虱的抗性。此外，我们证明本氏烟草毛状体中BCKD和IPMS-C的较高表达水平有助于O-AS的合成，从而增强对烟粉虱的抗性。此外，在栽培烟草烟草中过表达NbBCKD和NbIPMS-C基因增强了其对烟粉虱的抗性。我们的研究揭示了本氏烟草对烟粉虱致死作用的代谢和分子机制，并为提高对烟粉虱的抗性提供了一条有前景的途径。
