Hegedus Dwayne D, Rimmer S Roger
Agriculture and Agri-Food Canada, Molecular Genetics Section, 107 Science Place, Saskatoon, Saskatchewan, Canada S7N 0X2.
FEMS Microbiol Lett. 2005 Oct 15;251(2):177-84. doi: 10.1016/j.femsle.2005.07.040.
Sclerotinia sclerotiorum is unusual among necrotrophic pathogens in its requirement for senescent tissues to establish an infection and to complete the life cycle. A model for the infection process has emerged whereby the pathogenic phase is bounded by saprophytic phases; the distinction being that the dead tissues in the latter are generated by the actions of the pathogen. Initial colonization of dead tissue provides nutrients for pathogen establishment and resources to infect healthy plant tissue. The early pathogenicity stage involves production of oxalic acid and the expression of cell wall degrading enzymes, such as specific isoforms of polygalacturonase (SSPG1) and protease (ASPS), at the expanding edge of the lesion. Such activities release small molecules (oligo-galacturonides and peptides) that serve to induce the expression of a second wave of degradative enzymes that collectively bring about the total dissolution of the plant tissue. Oxalic acid and other metabolites and enzymes suppress host defences during the pathogenic phase, while other components initiate host cell death responses leading to the formation of necrotic tissue. The pathogenic phase is followed by a second saprophytic phase, the transition to which is effected by declining cAMP levels as glucose becomes available and further hydrolytic enzyme synthesis is repressed. Low cAMP levels and an acidic environment generated by the secretion of oxalic acid promote sclerotial development and completion of the life cycle. This review brings together histological, biochemical and molecular information gathered over the past several decades to develop this tri-phasic model for infection. In several instances, studies with Botrytis species are drawn upon for supplemental and supportive evidence for this model. In this process, we attempt to outline how the interplay between glucose levels, cAMP and ambient pH serves to coordinate the transition between these phases and dictate the biochemical and developmental events that define them.
核盘菌在坏死营养型病原体中较为特殊，它需要衰老组织来建立感染并完成生命周期。一种感染过程模型已经形成，即致病阶段被腐生阶段所界定；区别在于后者中的死亡组织是由病原体的作用产生的。对死亡组织的初始定殖为病原体的建立提供营养，并为感染健康植物组织提供资源。早期致病阶段涉及草酸的产生以及细胞壁降解酶的表达，例如在病斑扩展边缘的多聚半乳糖醛酸酶（SSPG1）和蛋白酶（ASPS）的特定同工型。这些活动释放出小分子（寡聚半乳糖醛酸和肽），这些小分子用于诱导第二轮降解酶的表达，这些降解酶共同导致植物组织的完全溶解。草酸和其他代谢物及酶在致病阶段抑制宿主防御，而其他成分引发宿主细胞死亡反应，导致坏死组织的形成。致病阶段之后是第二个腐生阶段，向该阶段的转变是由葡萄糖可用时cAMP水平下降以及进一步的水解酶合成受到抑制所实现的。低cAMP水平和草酸分泌产生的酸性环境促进菌核发育和生命周期的完成。本综述汇集了过去几十年收集的组织学、生化和分子信息，以建立这种三相感染模型。在几个实例中，借鉴了葡萄孢属物种的研究来为该模型提供补充和支持证据。在此过程中，我们试图概述葡萄糖水平、cAMP和环境pH之间的相互作用如何协调这些阶段之间的转变，并决定定义它们的生化和发育事件。
