Research on the mechanisms involved in pathogenicity and induction of defense reaction by plant pathogenic bacteria.

我们发现Phop-PhoQ双组分调控系统负责过度诱导果胶裂解酶，果胶裂解酶是胡萝卜欧文氏亚种的主要毒力因子。这种超诱导的刺激物是低pH、低浓度的糖、低浓度的镁和醋酸盐，它们被认为是相当于植物细胞内空间的环境。这一发现将对抗病作物的构建具有重要意义。此外，我们还发现avrBs3/pthgene家族对Harpin等通用激发子诱导的HR具有抑制活性。我们发现，Acidovorax venae对水稻品种的识别需要免疫系统的诱导和III型分泌系统的调节。我们还发现鞭毛的结构域位于鞭毛的C端病变中。此外，我们还从识别鞭毛的植物蛋白中分离出了功能未知的FIP50蛋白，并鉴定了调控根癌农杆菌接种的胆汁组织中端粒酶表达的AtBBF1和AtBBF2。在证实被称为端粒酶抑制素的抑制剂对植物端粒酶活性有抑制作用后，我们发现该抑制剂诱导的细胞凋亡与HR的发育同时出现。Atbi-1是细胞凋亡相关基因之一，在HR发育过程中抑制细胞凋亡的诱导。Bax抑制剂和HC毒素还原酶抑制HR细胞凋亡。

We found that PhoP-PhoQ two component regulatory system is responsible for the hyperinduction of pectate lyase that is the main virulent factor in Erwinia carotovora subsp.carotovora. The stimuli for this hyperinduction were low pH, low concentration of sugars, low concentration of magnesium, and acetate which are thought to be equivalent to the environment in plant intracellular space. This finding will be important traits for the construction of disease resistant crops. Also, we found that avrBs3/pthgene family has suppressor activity on HR induced by general elicitors such as harpin.We found that the induction of immune system and the regulation by type III secretion system are required for the recognition of rice cultivars by Acidovorax avenae. We also found that the domain of flagella resides in C-ending lesion of flagella. Furthermore, we have isolated the protein called FIP50 whose function is not known yet from the search of plant proteins recognizing the flagella.We have identified AtBBF1 and AtBBF2 which regulate the expression of telomerase in the gall tissues inoculated with Agrobacterium tumefaciens. After confirmation of the inhibitor called as telomestatin is effective in inhibiting the plant telomerase activity, we found that this inhibitor induce the apoptosis appearing simultaneously with HR development. The AtBI-1, one of apoptosis-related genes, was found to suppress the induction of apoptosis during HR development. Finally, Bax inhibitor and reducing enzyme of HC toxins inhibit the HR apoptosis.