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Sclerotinia sclerotiorum pathogenicity factors: Regulation and interaction with the host.

机译:核盘菌核盘菌致病性因素:调节和与宿主的相互作用。

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摘要

Sclerotinia sclerotiorum infects over 400 plant species. The pathogen employs several mechanisms to overcome plant defenses including the production of oxalic acid which suppresses the hypersensitive response.It also utilizes hydrolytic enzymes to degrade cell structure and necrosis-inducing molecules to cause cell death. The work described in this thesis: 1) identified and elucidated the role of select proteins and enzymes in S. sclerotiorum pathogenesis, 2) determined how their respective genes were regulated throughout the different stages of the infection, and 3) examined their interaction with plant defenses.;Beneath the cuticle, host integrity is maintained by layers of polysaccharides in the plant cell wall. S. sclerotiorum produces a suite of pectin degrading enzymes, and a gene encoding a novel endopolygalacturonase (PG), SsPg2, is described. While SsPg2 was not expressed during infection of B. napus, the expression pattern of SsPg1indicated that it was involved in infection initiation and lesion expansion. SsPg1expression was regulated by a complex network involving feedback inhibition by galacturonic acid, ambient pH, and carbon availability. Two S. sclerotiorum PGs were demonstrated to induce necrosis in the host. This activity was inhibited by the B. napus polygalacturonase inhibitor proteins BnPGIP1 and BnPGIP2; however, expression of a single BnPGIP in transgenic plants was insufficient to provide practical resistance.;This study also identified two S. sclerotiorum Necrosis and Ethylene-inducing Peptides (NEPs) that caused necrotic lesions to form in host plants. SsNep2 was expressed at a higher level than SsNep1 during infection of B. napus and in both the necrotic zone and the leading margin, indicating that it is involved in lesion expansion and the later necrotic stage.;The signaling mechanisms that are involved in regulating the expression of these pathogenicity-related genes were examined, these included cAMP, Ca + flux, calcineurin and mitogen activated protein kinases (MAPKs). Disruption of the Smk3, the orthologue of the Slt cell wall integrity MAPK gene from Saccharomyces cerevisiae, led to loss of virulence on intact B. napus leaves, but not on leaves stripped of cuticle. This phenotype appeared to be associated with alterred mycelial polarity, branching and hydrophobicity and inability to form infection cushions.;The plant surface is covered by a waxy layer referred to as the cuticle. A gene encoding a cutinase was identified in the S. sclerotiorum genome. SsCutA was expressed after mycelia were placed in contact with the cuticle or other solid surfaces. Expression was limited to the very early stages of the infection suggesting that the enzyme only plays a role in cuticle penetration.;In summary, this study examined the integration and coordination of multiple S. sclerotiorium pathogencity factors during the infection and their interaction with the host.
机译:核盘菌核盘菌感染400多种植物。该病原体采用多种机制来克服植物防御机制,包括产生草酸来抑制超敏反应,还利用水解酶降解细胞结构和诱导坏死的分子导致细胞死亡。本论文中描述的工作:1)鉴定并阐明了选择蛋白和酶在核盘菌中的作用; 2)确定了在感染的不同阶段如何调节各自的基因; 3)检查了它们与植物的相互作用。角质层下方,植物细胞壁中的多糖层保持宿主的完整性。核盘菌产生一套果胶降解酶,并描述了编码新型内聚半乳糖醛酸酶(PG)SsPg2的基因。尽管在甘蓝型油菜的感染过程中未表达SsPg2,但SsPg1的表达模式表明它与感染的起始和病变的扩展有关。 SsPg1的表达受一个复杂的网络调节,该网络涉及半乳糖醛酸,环境pH和碳的利用率对反馈的抑制作用。证实了两种S.sclerotiorum PGs在宿主中诱导坏死。甘蓝型油菜聚半乳糖醛酸酶抑制剂蛋白BnPGIP1和BnPGIP2抑制了这种活性。然而,在转基因植物中表达单个BnPGIP不足以提供实际的抗性。该研究还确定了导致宿主植物中形成坏死病灶的两种葡萄球菌坏死和乙烯诱导肽(NEP)。在甘蓝型油菜感染期间以及坏死区和前缘中SsNep2的表达水平均高于SsNep1,这表明它与病灶扩展和晚期坏死阶段有关。检查了这些致病性相关基因的表达,包括cAMP,Ca +通量,钙调神经磷酸酶和丝裂原活化蛋白激酶(MAPK)。来自酿酒酵母的Slt细胞壁完整性MAPK基因的直向同源物Smk3的破坏导致完整的甘蓝型油菜叶片(而不是表皮剥离的叶片)的毒力丧失。该表型似乎与改变的菌丝体极性,分支和疏水性以及不能形成感染垫有关。植物表面被称为表皮的蜡质层覆盖。在菌核盘菌基因组中鉴定了编码角质酶的基因。将菌丝体与表皮或其他固体表面接触后表达SsCutA。表达仅限于感染的早期阶段,表明该酶仅在角质层渗透中起作用。总之,本研究检查了感染过程中多种葡萄球菌致病因子的整合和协调及其与宿主的相互作用。 。

著录项

  • 作者

    Dallal Bashi, Zafer.;

  • 作者单位

    The University of Saskatchewan (Canada).;

  • 授予单位 The University of Saskatchewan (Canada).;
  • 学科 Biology Molecular.;Agriculture Plant Pathology.
  • 学位 Ph.D.
  • 年度 2011
  • 页码 174 p.
  • 总页数 174
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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