【摘要】 硫酸二乙酯（DES）化学诱变水稻细条斑病菌（Xanthomonasoryzaepv.oryzicola）RS105获得6株hrp突变体，其在寄主水稻上失去致病性和在非寄主烟草上失去激发过敏反应（hypersensitiveresponse，HR）的能力。将水稻白叶枯病菌（X．oryzaepv．oryzae）日本系统Ⅲ号小种（JXOⅢ）基因文库和RS105基因文库互补RS105hrp突变体M55，分别得到来自JXOⅢ的阳性克隆pUHRX245和来自RS105的阳性克隆pUHRS130、PUHRS138和PUHRS662。所有功能互补子都和野生型菌株RS105一样，能在非寄主烟草上激发HR，但在寄主水稻上，仅有4个互补子M1005／pUHRX245、M1005／pUHRS130、M1005／pUHRS138和M1005／pUHRS662恢复了致病性。生化和细胞组分测定结果表明，RS105、hrp突变体和其功能互补子的胞外酶（淀粉酶、蛋白酶、果胶酶、纤维素酶和脂酶）活性基本一致，激发非奇主烟草产生HR的信号物质不是LPS，而是harpin类蛋白，hrp突变体M51、M1016和M1098为Ⅲ型泌出通道突变体，hrp突变体M55、M1005和M1198可能为编码和调控harpin类蛋白的突变体。更多还原

【Abstract】 6 strains of hrp mutants, losing their pathogenicity on susceptible rice, Shanyou 63, and ability to trigger hypersensitive response (HR) on nonhost plant, tobacco, were obtained from wild type RS105 of Xanthomonas oryzae pv. oryzicola (Xooc) by using DiethyI sulfate (DES) as a mutagenic chemical. 4 hrp gene clones, pUHRX245 from X. o. pv. oryzae (Xoo) gene library and pUHRS130, pUHRS138 and pUHRS662 from Xooc gene library could restore all the hrp mutants the ability to trigger HR on tobacco by functional complementation method, but only hrp mutant M1005 could be restored to the wild type RS105 on the rice.Biochemical and cellular composition analyses demonstrated thatthe extracellularenzyme (amylase, pectate lyase, protease, cellulaseand lipase) activities of all the hrp mutants and their functional conjugates were homogeneous to those of the wild typc. Harpin-like protein, but not lipopolysaccharide (LPS) was the substance that elicited HR on tobacco and that could be detected in sonicated cells and supernatant of the sonicated cells of the wild type RS105 and hrp mutants M51. M 1016 and M 1098. It was suggested that hrpmutants, M51, M 1016 and M 1098 were inutated in type Ⅲ secretion pathway, and that hrp mutant M55, M 1005 and M1198 were altered in sequences encoding or regulating harpin-like protein.更多还原