摘要
以抗稻瘟病水稻近等基因系C101LAC及背景品系CO39为材料,研究稻瘟菌 (Magnaporthegrisea)来源的GP66激发子诱导的水稻膜脂过氧化及保护酶活性变化。结果表明,激发子诱导非亲和性互作水稻超氧阴离子 (O-2· )积累和脂氧合酶(LOX)活性在早期明显高于亲和性互作水稻;O-2·积累和LOX活性的升高进而导致了非亲和性互作水稻的膜脂过氧化,其相对电导率及丙二醛(MDA)含量出现的高峰期和强度也明显要早和高于亲和性互作水稻。超氧化物歧化酶 (SOD)和过氧化氢酶(CAT)活性均趋于下降,不同亲和性互作水稻间的变化则不明显;非亲和性互作水稻过氧化物酶 (POD)活性则在激发子诱导早期明显高于亲和性互作水稻,可能与其参与其它抗性有关。这些结果表明膜脂过氧化的发生是激发子诱导水稻抗性的主要生理机制之一。
Activation of membrane lipid peroxidation and defense enzymes was investigated on both incompatible and compatible rice leaves treated with M. grisea- derived elicitor GP66. Compared with the compatible rice,the GP66 treatment caused rapid and remarkable O - 2 ·generation and an increasing of lipoxygenase (LOX) activity in incompatible rice leaves. These changes further led to lipid peroxidation,concomitant with an increasing of the relative conductance rate and an accumulation of the maloondiadehyde (MDA). Peroxidase (POD) was also stimulated in the early stage of the incompatible reaction. By contrast,treatment of GP66 caused a decline of superoxide dismutase (SOD) activity and catalase (CAT) activity in both compatible and incompatible rice cultivars. The results suggest that lipid peroxidation in rice leaves induced by GP66 elicitor may play an important role in the resistance of rice seedlings.
出处
《植物病理学报》
CAS
CSCD
北大核心
2005年第1期43-48,共6页
Acta Phytopathologica Sinica
基金
广东省自然科学基金重点课题资助项目(010350)