西瓜专化型尖孢镰刀菌FonSIX6缺失突变体的构建

Construction of FonSIX6 deletion mutant of Fusarium oxysporum f.sp.niveurn

病原菌和植物相互作用时分泌效应蛋白(effectors)抑制植物的防卫反应。枯萎病是由尖孢镰刀菌引起的真菌病害,尖孢镰刀菌和寄主相互作用时分泌几个特定的富含半胱氨酸的小分子量蛋白(15.8～29.9kD)进入木质部启动致病力,称为SIX(secreted in xylem)蛋白,其中,SIX6蛋白是一个效应蛋白。西瓜枯萎病是由西瓜专化型尖孢镰刀菌(Fusarium oxysporum f.sp.Niveurn,Fon)引起的真菌病害。为了明确FonSIX6在侵染西瓜时的作用,克隆了该基因的上下游序列,以潮霉素为筛选标记构建了该基因的缺失突变体载体pDH-SIX6;将构建好的基因缺失载体转入农杆菌AGL-1中,通过农杆菌介导的遗传转化和转化子的筛选获得了FonSIX6基因的缺失突变体。

Abstract： During the interactions between plant pathogen and host plant, the pathogen secretes effector protein to suppress host defenses. Fusarium wilt is a fungal disease caused by Fusarium oxysporum,the fungus secretes several effector proteins into the plant xylem to promote virulence. These effectors are small molecular cysteine-rich proteins and called SIX（ secreted in xylem）proteins, and the SIX6 was one of them. Fusrium wilt of watermelon was a patho- genic fungus caused by Fusarium oxysporum f. sp. niveurn（Fort）. To understand the function of FonSIX6 during in- fection,the flanking region of FonSIX6 was cloned and the deletion mutant vector of FonSIX6 with hygromyein was constructed as a selectable marker. The constructed gene deletion vector was transferred into Agrobacterium stain AGL-1 and then FonSIX6 deletion mutant was obtained by Agrobacterium-mediated transformation system.