Extracellular RNAs in vascular wilt diseases

引起维管萎蔫的病原体是最具破坏性的植物丝之一。大多数土传的卵菌、细菌或真菌定殖于导水的木质部导管，这导致水分供应受损、萎蔫，并最终导致植物死亡。维管枯萎病和宿主防御反应的分子基础还不清楚，主要是因为病原体驻留在其宿主植物的内部，不容易接近。在这个项目中，我们希望主要集中在甘蓝型油菜-长孢轮枝菌相互作用作为一个研究系统，因为它允许评估植物脉管系统作为宿主-真菌战场。此外，还比较了苛养木杆菌和长孢木霉菌感染对拟南芥质外体反应的影响。本研究的目的是阐明油菜科植物与枯萎病病原菌相互作用中胞外RNA - RBP复合物交换的分子机制。该研究围绕以下问题展开：（a）植物宿主和维管枯萎病病原体之间的细胞外RNA交换如何参与感染过程，（B）细胞外RNA和RNA-RBP复合物如何在宿主和病原体之间靶向和交换。我们的研究将揭示如果胞外RNA和RNA-RBP复合物发挥作用的相互作用的兰科植物与真菌和细菌的维管枯萎病病原体。结合联盟中其他项目的见解，我们努力寻找增加植物抗性的新方法。

Pathogens inducing vascular wilts are among the most destructive plant threads. The mostly soil-borne oomycetes, bacteria, or fungi colonize the water-conducting xylem vessels what leads to impairment of water supply, wilting, and eventually plant death. The molecular basis underlying vascular wilt diseases and host defense reactions is not well understood, mainly because the pathogens reside in the interior of their host plants and are not easy to access. In this project we want to focus mainly on the Brassica napus - Verticillium longisporum interaction as a research system, because it allows assessing the plant vasculature as the host-fungus battleground. In addition, effects of Xylella fastidiosa and V. longisporum infection on the apoplastic response in Arabidopsis will be compared. The goal of this strategy is to elucidate the molecular mechanism of the exchange of extracellular RNA – RBP complexes in the interaction between Brassicaceae and vascular wilt pathogens. The research is centered around the questions (a) how extracellular RNA exchange between plant host and vascular wilt pathogens is involved in the infection process, (b) how extracellular RNAs and RNA-RBP complexes can be targeted and exchanged between hosts and pathogens. Our studies will reveal if extracellular RNAs and RNA-RBP complexes play a role in the interaction of Brassicaceae plants with a fungal and a bacterial vascular wilt pathogen. Combined with the insights from the other projects in the consortium, we strive for finding novel ways to increase plant resistance.