H_2O_2、NO和Ca^(2+)参与疫病菌激发子PB90诱导烟草气孔的关闭

Hydrogen peroxide,nitro oxide and calcium participated in stomatal closure induced by elicitor PB90 from Phytophthora boehmeriae

本文研究了过氧化氢(H2O2)、一氧化氮(NO)和Ca2+在棉疫病菌激发子PB90诱导烟草气孔运动中的作用。1nm o l/L激发子PB90可诱导野生型烟草Bel-W 3气孔关闭,且在相同条件下该激发子诱导反义抑制抗坏血酸过氧化物酶anti-APX烟草气孔关闭的孔径比野生型的更小;进一步药理学证明,抗氧化剂DTT和NADPH氧化酶抑制剂DPI(d ipheny-lene iodonium)、一氧化氮合酶(NO S)抑制剂L-NAM E、Ca2+螯合剂EGTA和Ca2+信号途径中CaM PKⅡ的竞争抑制剂KN93与磷脂酶C抑制剂U73122都能抵消PB90诱导气孔关闭的效应。推测该激发子PB90通过NADPH氧化酶途径形成H2O2、NO S途径形成NO和Ca2+信号途径进而诱导气孔关闭。表明H2O2、NO、Ca2+在激发子PB90诱导气孔关闭信号传递中作为第二信使起着重要的作用。

The role of hydrogen peroxide （H2O2）, nitro oxide （NO） and calcium （Ca^2＋） in stomatal closure of tobacco induced by elicitor PB90, a protein elicitor secreted by Phytophthora boehmeriae was investigated. Treatment to abaxial surface of young expanded leaves with 1 nmol/L PB90 could induce stomatal closure in wild-type tobacco cv. Bel-W3. Transgenic anti-APX tobacco could produce more H2O2 than Bel-W3 after treatment with PB90 and stomatal aperture of anti-APX was smaller than that of wild-type tobacco. Further experiments revealed that pretreatment with DTT, an antioxidant, DPI, an inhibitor of NADPH oxidase, L-NAME, an inhibitor of nitro oxide synthase, EGTA, a Ca^2＋ specific chelate, KN93, a competitively inhibitor of CaMPK Ⅱ, and U73122, an inhibitor of phospholipase C were able to attenuate PB90-triggered stomatal closure of wild-type tobacco. It was suggesting that PB90 induced stomatal closure involving H2O2 production via NADPHase, NO generation via nitro oxide synthase and Ca^2＋ signal transduction pathway and the molecules such as H2O2, NO and Ca^2＋ functioned as the second signals involved in PB90-induced stomatal closure.