印度梨形孢诱导烟草的抗病性分析

Disease Resistance Analysis of Nicotiana tabacum Induced by Piriformospora indica

内生真菌印度梨形孢(Piriformospora indica)能够增强植物体抗生物和非生物胁迫能力。为了明确印度梨形孢对诱导烟草抗病性的作用,分别进行了接种病原菌长柄链格孢、胶孢炭疽菌、终极腐霉和茄丝核菌后印度梨形孢定殖的烟草对赤星病、炭疽病、猝倒病和立枯病害的抗性试验,同时分析了接种长柄链格孢后烟叶中丙二醛(MDA)和脯氨酸(Pro)含量、抗氧化酶活性以及病程相关蛋白基因表达水平。结果表明:印度梨形孢定殖的烟草,接种长柄链格孢后,烟叶病斑显著减小,烟叶中MDA含量显著降低,Pro含量显著升高,病程相关蛋白基因PR-1a,PR2,PR3和PR5的表达量明显提高;接种胶孢炭疽菌后,烟叶病斑减小;终极腐霉和茄丝核菌对烟草的危害症状显著减轻。印度梨形孢能诱导烟草产生抗病性,是通过维持生物膜系统的完整性、稳定细胞内渗透压以及膜脂过氧化在较低水平、并调控病程相关蛋白基因的表达来实现的。

Piriformospora indica （P.indica）,a root-colonizing endophytic fungus,can improve the resistance of plants against biotic and abiotic stresses.In order to clarify the influences of P.indica on the disease resistance of Nicotiana tabacum,the resistance experiments against tobacco brown spot,anthracnose,damping off and sore shin were conducted wherein P.indica-colonized N.tabacum was inoculated with Alternaria longipes （A.longipes）,Colletotrichum gloeosporioides （C.gloeosporioides）,Pythium ultimum （P.ultimum） and Rhizoctonia solani （R.solani）,respectively; and the contents of malondialdehyde （MDA） and proline,antioxidant enzyme activity and the expression levels of pathogenesis-related protein genes in tobacco leaves inoculated with A.longipes were analyzed.The results showed that comparing with the control,the size of disease spots and the MDA content in the leaves of P.indica-colonized N.tabacum inoculated with A.longipes reduced significantly,while the proline content and the expression levels of pathogenesis-related protein genes PR-1a,PR2,PR3 and PR5 increased significantly; the size of disease spots in the leaves of P.indica-colonized N.tabacum inoculated with C.gloeosporioides reduced; and damage symptoms of the leaves of P.indica-colonized N.tabacum inoculated with P.ultimum and R.solani significantly decreased.P.indica can improve the disease resistance of N.tabacum through maintaining the integrity of cell biomembrane system,keeping intracellular osmotic pressure and the peroxidation of membrane lipid at a lower level and regulating the expression of pathogenesis-related protein genes.