G蛋白调控植物抗性的分子机制研究

The hypersensitive response (HR), a form of programmed cell death (PCD), is a tightly regulated innate immune response in plants, which is hypothesized to restrict pathogen growth and disease development. But the initiation and modulation of HR remains largely unknown and requires deep investigation. Previous reports from our group focused on two family members NbERD2a/2b to dissect their function on the modulation of cell death.For further understanding the molecular mechanism of ERD2s-mediated cell death, this study will demonstrate that plant G protein can interact with ERD2s and participate in ERD2s-mediated ER retrieval. We will also determine the function of G protein on non-host pathogens Xanthomonas oryzae pv. oryzae (Xoo) and Pseudomonas syringae pv. tomato DC3000 (Pst DC3000)-induced HR. We will prove that ERD2s-G signaling pathway is important for HR cell death regulation. Our research will establish the relationship and the molecular mechanism that endomembrane system G protein, not the plasma membrane fraction, can function in the plant non-host resistance, providing novel insights into the understanding the plant resistance.

植物抗病过程常伴随超敏反应，在病原侵染点及其周围的细胞发生程序性死亡。超敏反应被认为用于限制病原的增殖和病害的进一步发展，但超敏反应发生和调控机制仍不清楚，有待深入研究。前期工作表明内膜信号系统中ERD2a/2b两个同源蛋白对细胞死亡具有调控作用。为了研究ERD2s介导细胞死亡的分子机制，我们寻找与ERD2s互作的蛋白，初步结果表明G蛋白亚基能与这两个蛋白互作，本研究将进一步证明植物G蛋白亚基能够与ERD2s互作并参与ERD2s介导的内质网回流；并证明G蛋白亚基能够对非宿主病菌Xanthomonas oryzae pv. oryza及Pseudomonas syringae pv. tomato DC3000诱导的超敏反应具有调控作用，探讨G蛋白信号通路和 ERD2s对细胞死亡的调控机制。本研究将建立位于内膜系统而非细胞质质膜上的G蛋白对于非宿主抗性调控的分子机制，具有重要的理论意义。