Manipulation of the Xanthophyll Cycle Increases Plant Susceptibility to Sclerotinia sclerotiorum.
Manipulation of the Xanthophyll Cycle Increases Plant Susceptibility to Sclerotinia sclerotiorum.
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DOI：
10.1371/journal.ppat.1004878
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发表时间：
2015-05
期刊：
影响因子：
6.7
通讯作者：
Xing D
中科院分区：
文献类型：
--
作者：
Zhou J;Zeng L;Liu J;Xing D
在叶绿素荧光非光化学猝灭（NPQ）过程中，叶黄素循环参与了耗散多余光能以保护光合装置的过程。在感染的早期，叶黄素循环受到坏死性病原菌菌核菌的调节。即使在低光强条件下，菌核菌的培养也会导致NPQ的局部增加。进一步研究表明，NPQ的异常变化与菌核菌分泌的草酸盐引起的pH降低密切相关，这可能导致ATP合酶活性降低，导致类囊体腔在持续光照下酸化加深。此外，紫黄质去环氧化酶（VDE）的抑制（使用二硫苏糖醇）或缺陷（在npq1-2突变体中）消除了菌核菌诱导的NPQ增加。高效液相色谱分析表明，接种菌核菌的组织积累了大量的玉米黄质，而紫黄质含量则相应减少。免疫分析显示，这些叶黄素前体的减少减少了新生脱落酸（ABA）的生物合成，并明显减弱了组织防御反应，包括ROS诱导和胼胝质沉积，导致植物对菌核病的敏感性增强。因此，我们提出在早期发病过程中，菌核菌通过控制叶黄素循环，拮抗ABA生物合成来抑制宿主防御。这些发现为光保护代谢产物如何整合到防御反应中提供了一个模型，并扩展了目前关于感染部位早期植物-菌核菌相互作用的知识。近年来，叶绿体在植物与微生物相互作用和光合作用研究中的作用得到了广泛的研究。众所周知，叶黄素循环在叶绿素荧光的非光化学猝灭（NPQ）过程中参与了耗散多余光能以保护光合装置。最近的研究表明，NPQ可能受到病原体攻击的积极或消极影响。然而，关于病原体影响NPQ的调控过程以及它们对植物防御反应的影响的知识是不完整的。研究了坏死性菌核病侵染拟南芥叶片对叶黄素循环的影响。我们的研究首次揭示了菌核菌使用一种涉及操纵叶黄素循环的新策略来削弱宿主防御反应并增加其在宿主细胞中的成功定植。这些发现有助于了解植物与菌核菌在早期发病机制中的相互作用，为开发提高植物菌核菌抗性的策略提供新的视角，以供实际应用。
The xanthophyll cycle is involved in dissipating excess light energy to protect the photosynthetic apparatus in a process commonly assessed from non-photochemical quenching (NPQ) of chlorophyll fluorescence. Here, it is shown that the xanthophyll cycle is modulated by the necrotrophic pathogen Sclerotinia sclerotiorum at the early stage of infection. Incubation of Sclerotinia led to a localized increase in NPQ even at low light intensity. Further studies showed that this abnormal change in NPQ was closely correlated with a decreased pH caused by Sclerotinia-secreted oxalate, which might decrease the ATP synthase activity and lead to a deepening of thylakoid lumen acidification under continuous illumination. Furthermore, suppression (with dithiothreitol) or a defect (in the npq1-2 mutant) of violaxanthin de-epoxidase (VDE) abolished the Sclerotinia-induced NPQ increase. HPLC analysis showed that the Sclerotinia-inoculated tissue accumulated substantial quantities of zeaxanthin at the expense of violaxanthin, with a corresponding decrease in neoxanthin content. Immunoassays revealed that the decrease in these xanthophyll precursors reduced de novo abscisic acid (ABA) biosynthesis and apparently weakened tissue defense responses, including ROS induction and callose deposition, resulting in enhanced plant susceptibility to Sclerotinia. We thus propose that Sclerotinia antagonizes ABA biosynthesis to suppress host defense by manipulating the xanthophyll cycle in early pathogenesis. These findings provide a model of how photoprotective metabolites integrate into the defense responses, and expand the current knowledge of early plant-Sclerotinia interactions at infection sites. In recent years, the role of the chloroplast in the defense against microbes has been intensively investigated and is of high interest to both plant-microbe interaction and photosynthesis research. The xanthophyll cycle is well known to be involved in dissipating excess light energy to protect the photosynthetic apparatus in a process commonly assessed via non-photochemical quenching (NPQ) of chlorophyll fluorescence. Recent studies show that NPQ can be positively or negatively affected by pathogen attack. However, knowledge about the regulatory processes by which pathogens affect NPQ, as well as their impact on plant defense responses, is incomplete. This work characterized the impact of infection of Arabidopsis leaves by the necrotrophic pathogen Sclerotinia sclerotiorum on the xanthophyll cycle. Our research revealed for the first time that Sclerotinia uses a novel strategy involving manipulation of the xanthophyll cycle to weaken host defense responses and increase its successful colonization of host cells. These findings contribute to understanding the plant-Sclerotinia interactions in early pathogenesis, which will provide new sights into the development of strategies to increase Sclerotinia resistance in plants for practical applications.
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