Contribution of Ethylene Biosynthesis for Resistance to Blast Fungus Infection in Young Rice Plants

                6.125
                Takayoshi Iwai, Atsushi Miyasaka, Shigemi Seo, Yuko Ohashi
                Plant Physiology, 2006, 142(3): 1202-1215     追溯原文......本站官方QQ群:62473826

                The role of ethylene (ET) in resistance to infection with blast fungus (Magnaporthe grisea) in rice (Oryza sativa) is poorly understood. To study it, we quantified ET levels after inoculation, using young rice plants at the four-leaf stage of rice cv Nipponbare (wild type) and its isogenic plant (IL7), which contains the Pi-i resistance gene to blast fungus race 003. Small necrotic lesions by hypersensitive reaction (HR) were formed at 42 to 72 h postinoculation (hpi) in resistant IL7 leaves, and whitish expanding lesions at 96 hpi in susceptible wild-type leaves. Notable was the enhanced ET emission at 48 hpi accompanied by increased 1-aminocyclopropane-1-carboxylic acid (ACC) levels and highly elevated ACC oxidase (ACO) activity in IL7 leaves, whereas only an enhanced ACC increase at 96 hpi in wild-type leaves. Among six ACC synthase (ACS) and seven ACO genes found in the rice genome, OsACS2 was transiently expressed at 48 hpi in IL7 and at 96 hpi in wild type, and OsACO7 was expressed at 48 hpi in IL7. Treatment with an inhibitor for ACS, aminooxyacetic acid, suppressed enhanced ET emission at 48 hpi in IL7, resulting in expanding lesions instead of HR lesions. Exogenously supplied ACC compromised the aminooxyacetic acid-induced breakdown of resistance in IL7, and treatment with 1-methylcyclopropene and silver thiosulfate, inhibitors of ET action, did not suppress resistance. These findings suggest the importance of ET biosynthesis and, consequently, the coproduct, cyanide, for HR-accompanied resistance to blast fungus in young rice plants and the contribution of induced OsACS2 and OsACO7 gene expression to it.

                乙烯生物合成對水稻幼苗稻瘟病抗性的作用

                對于乙烯(ET)在水稻稻瘟病抗性中的作用目前了解的還很少。本研對四葉期日本晴幼苗和包含Pi-i基因(抗稻瘟病003小種)的近等基因系(IL7)幼苗進行接菌,定量分析接種后植株體內ET水平。IL7抗性植株葉片在接菌后(hpi)42-72h超敏反應產生小壞死斑,感病的野生型葉片在96hpi產生泛白的擴展病斑。值得注意的是,IL7葉片在48 hpi ET釋放增加,同時伴隨1-氨基環(huán)丙烷-1-羧酸(ACC)水平的升高和ACC氧化酶(ACO)活性的增強,而野生型葉片只在96 hpi有ACC的增加。水稻基因組6個ACC合酶基因(ACS)和7個ACO中, OsACS2在IL7中48 hpi、野生型中96 hpi短暫表達,OsACO7在IL7中48 hpi表達。用ACS的抑制劑氨氧基乙酸處理IL7,ET在48 hpi的釋放受到抑制,擴展型病斑取代了HR病斑的形成。施加外源ACC抑制了氨氧基乙酸處理導致的IL7抗性喪失,而用ET活性抑制劑1-甲基環(huán)丙烯和硫代硫酸銀處理則不能抑制抗性。這些數(shù)據表明ET的生物合成及其副產物氰化物對水稻幼苗伴隨超敏反應的稻瘟病抗性是十分重要的,另外OsACS2和OsACO7基因的誘導表達對稻瘟病抗性也是有作用的。


                基因列表
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO1; OsACO2
                  1-氨基環(huán)丙烷-1-羧酸氧化酶 OsACO7
                  1-氨基環(huán)丙烷-1-羧酸合酶 OsACS2
                  1-氨基環(huán)丙烷-1-羧酸合酶基因 OsACS1
                  1-氨基環(huán)丙烷-1-羧酸合酶 OsACS5
                  氨基轉移酶 OsACS6; SSG6
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO2; OsACO1
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO3
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO4
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO5
                  1-氨基環(huán)丙烷-1-羧酸氧化酶基因 OsACO6
                  1-氨基環(huán)丙烷-1-羧酸合酶 OsACS3
                  1-氨基環(huán)丙烷-1-羧酸合酶 OsACS4
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