水稻类病变突变体spl5细胞坏死机制的分析

Mechanisms of cell death in rice lesion mimic muant spl5

水稻spl5(spotted leaf 5)属于起始型类病变突变体,植株从苗期开始叶片上就会自发地表现出红棕色类病斑.组织学染色和生理生化分析结果表明,spl5类病斑是由于活性氧(ROI)的过量积累引起细胞坏死或激活了程序性细胞死亡(PCD)途径所致.2种能诱导细胞死亡的活性氧在spl5类病斑形成部位有明显的积累,其中超氧离子基(O2-)含量的增加始于细胞坏死之前,而H2O2积累则在类病斑性状出现之后,表明ROI代谢的失调,尤其是O2-的过量积累可能是造成spl5细胞坏死的主要原因之一.由于分别专一催化O2-和H2O2分解的超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性在类病斑形成过程中也相应提高,说明spl5突变体内ROI清除酶系功能正常.

spl5 mutant （ spotted leaf 5 ）, an initiation-type lesion mimic, spontaneously displays small reddish brown spots in leaves at seedling stages. Histochemical and physiological analyses showed that the phenotype of spl5 resulted from activation of programmed cell death （ PCD ） and necrosis by reactive oxygen intermediates （ROI） excessive accumulation. Two species of ROI, superoxide （O^-2 ） and H2O2, cell-death inducers, accumulated remarkably in the sites of spots. Superoxide increased prior to initiation of cell death in the leaves of spl5, whereas H2O2 did not accumulate until lesion formation. It showed that metabolic misregulation of ROI, especially excessive accumulation of superoxide, was one of the main reasons responsible for the cell death in the leaves of splS. Furthermore, an increase in the activities of superoxide dismutase （ SOD）and catalase （CAT） , specific scavengers for superoxide and H2O2, respectively, was observed in the course of lesion formation.