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Interactive Responses of Potato (Solanum tuberosum L.) Plants to Heat Stress and Infection With Potato Virus Y

机译：马铃薯（Solanum tuberosum L.）植物对热胁迫和马铃薯病毒Y感染的相互作用

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Potato (Solanum tuberosum) plants are exposed to diverse environmental stresses, which may modulate plant–pathogen interactions, and potentially cause further decreases in crop productivity. To provide new insights into interactive molecular responses to heat stress combined with virus infection in potato, we analyzed expression of genes encoding pathogenesis-related (PR) proteins [markers of salicylic acid (SA)-mediated plant defense] and heat shock proteins (HSPs), in two potato cultivars that differ in tolerance to elevated temperatures and in susceptibility to potato virus Y (PVY). In plants of cv. Chicago (thermosensitive and PVY-susceptible), increased temperature reduced PR gene expression and this correlated with enhancement of PVY infection (virus accumulation and symptom production). In contrast, with cv. Gala (thermotolerant and PVY resistant), which displayed a greater increase in PR gene expression in response to PVY infection, temperature affected neither PR transcript levels nor virus accumulation. HSP genes were induced by elevated temperature in both cultivars but to higher levels in the thermotolerant (Gala) cultivar. PVY infection did not alter expression of HSP genes in the Gala cultivar (possibly because of the low level of virus accumulation) but did induce expression of HSP70 and HSP90 in the susceptible cultivar (Chicago). These findings suggest that responses to heat stress and PVY infection in potato have some common underlying mechanisms, which may be integrated in a specific consolidated network that controls plant sensitivity to multiple stresses in a cultivar-specific manner. We also found that the SA pre-treatment subverted the sensitive combined (heat and PVY) stress phenotype in Chicago, implicating SA as a key component of such a regulatory network.
机译：马铃薯（Solanum tuberosum）植物暴露于多种环境胁迫下，这可能会调节植物与病原体的相互作用，并可能导致作物生产力进一步下降。为了提供对马铃薯热应激和病毒感染的相互作用分子反应的新见解，我们分析了编码致病相关（PR）蛋白[水杨酸（SA）介导的植物防御标记）和热休克蛋白（HSPs）的基因表达），这两个马铃薯品种对高温的耐受性和对马铃薯Y病毒（PVY）的敏感性不同。在简历中芝加哥（对热敏感且对PVY敏感），温度升高会降低PR基因的表达，这与PVY感染（病毒积累和症状产生）的增强相关。相反，与简历。 Gala（具有耐热性和PVY抵抗力）可响应PVY感染而显示PR基因表达的更大增加，温度既不会影响PR转录水平，也不会影响病毒积累。 HSP基因在两个品种中均由高温诱导，但在耐热（Gala）品种中却升高。 PVY感染不会改变Gala品种中HSP基因的表达（可能是由于病毒积累水平较低），但确实会诱导易感品种（芝加哥）中HSP70和HSP90的表达。这些发现表明，马铃薯对热胁迫和PVY感染的反应具有一些共同的潜在机制，这些机制可能整合在一个特定的整合网络中，该网络以特定品种的方式控制植物对多种胁迫的敏感性。我们还发现，SA预处理颠覆了芝加哥的敏感组合（热和PVY）应激表型，暗示SA是此类监管网络的关键组成部分。

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