Marina María, Maiale Santiago Javier, Rossi Franco Rubén, Romero Matías Fernando, Rivas Elisa Isabel, Gárriz Andrés, Ruiz Oscar Adolfo, Pieckenstain Fernando Luis
Universidad Nacional de General San Martín-Consejo Nacional de Investigaciones Científicas y Técnicas, B7130IWA Chascomus, Argentina.
Plant Physiol. 2008 Aug;147(4):2164-78. doi: 10.1104/pp.108.122614. Epub 2008 Jun 26.
The role of polyamine (PA) metabolism in tobacco (Nicotiana tabacum) defense against pathogens with contrasting pathogenic strategies was evaluated. Infection by the necrotrophic fungus Sclerotinia sclerotiorum resulted in increased arginine decarboxylase expression and activity in host tissues, as well as putrescine and spermine accumulation in leaf apoplast. Enhancement of leaf PA levels, either by using transgenic plants or infiltration with exogenous PAs, led to increased necrosis due to infection by S. sclerotiorum. Specific inhibition of diamine and PA oxidases attenuated the PA-induced enhancement of leaf necrosis during fungal infection. When tobacco responses to infection by the biotrophic bacterium Pseudomonas viridiflava were investigated, an increase of apoplastic spermine levels was detected. Enhancement of host PA levels by the above-described experimental approaches strongly decreased in planta bacterial growth, an effect that was blocked by a PA oxidase inhibitor. It can be concluded that accumulation and further oxidation of free PAs in the leaf apoplast of tobacco plants occurs in a similar, although not identical way during tobacco defense against infection by microorganisms with contrasting pathogenesis strategies. This response affects the pathogen's ability to colonize host tissues and results are detrimental for plant defense against necrotrophic pathogens that feed on necrotic tissue; on the contrary, this response plays a beneficial role in defense against biotrophic pathogens that depend on living tissue for successful host colonization. Thus, apoplastic PAs play important roles in plant-pathogen interactions, and modulation of host PA levels, particularly in the leaf apoplast, may lead to significant changes in host susceptibility to different kinds of pathogens.
评估了多胺（PA）代谢在烟草（Nicotiana tabacum）抵御具有不同致病策略病原体中的作用。坏死营养型真菌核盘菌（Sclerotinia sclerotiorum）感染导致宿主组织中精氨酸脱羧酶表达和活性增加，以及叶片质外体中腐胺和亚精胺积累。通过使用转基因植物或用外源多胺浸润来提高叶片多胺水平，会导致核盘菌感染引起的坏死增加。对二胺氧化酶和多胺氧化酶的特异性抑制减弱了真菌感染期间多胺诱导的叶片坏死增强。当研究烟草对活体营养型细菌绿黄假单胞菌（Pseudomonas viridiflava）感染的反应时，检测到质外体亚精胺水平增加。通过上述实验方法提高宿主多胺水平会强烈降低植物体内细菌生长，这种效应被多胺氧化酶抑制剂阻断。可以得出结论，在烟草抵御具有不同致病策略微生物感染的过程中，烟草植株叶片质外体中游离多胺的积累和进一步氧化以相似但不完全相同的方式发生。这种反应影响病原体在宿主组织中定殖的能力，结果对植物抵御以坏死组织为食的坏死营养型病原体的防御是有害的；相反，这种反应在抵御依赖活组织成功定殖宿主的活体营养型病原体的防御中发挥有益作用。因此，质外体多胺在植物 - 病原体相互作用中起重要作用，调节宿主多胺水平，特别是叶片质外体中的多胺水平，可能导致宿主对不同种类病原体易感性的显著变化。
