HCPro Suppression of Callose Deposition Contributes to Strain-Specific Resistance Against Potato Virus Y
HCPro Suppression of Callose Deposition Contributes to Strain-Specific Resistance Against Potato Virus Y
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DOI：
10.1094/phyto-07-19-0229-fi
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发表时间：
2020-01-01
期刊：
影响因子：
3.2
通讯作者：
Rakotondrafara, Aurelie M.
中科院分区：
文献类型：
--
作者：
Chowdhury, Rawnaq N.;Lasky, Danny;Rakotondrafara, Aurelie M.
马铃薯Y病毒（PVY;马铃薯Y病毒科（Potyviridae）是马铃薯生产的持续挑战，这是由于菌株特异性抗性品种的日益普及。超敏抗性是植物为抑制病毒传播而产生的一种防御反应。在许多马铃薯栽培品种中，例如栽培品种Premier Russet（PR），感染部位的局部坏死保护免受最常见的PVYO菌株的侵害，但HR通常不能抑制坏死菌株，其全身传播。在这里，我们建立了胼胝质积累的作用，在株系特异性抗PVY感染的反应。我们首先发现PVY，独立于菌株，是自然能够抑制易感宿主中的病程相关的胼胝质形成。这种活性可以通过病毒编码的辅助组分蛋白酶（HCPro）蛋白的瞬时表达而与病毒复制分离，将其鉴定为病原体激发子。然而，与坏死株不同的是，PVYO及其相应的HCPro无法阻止抗性PR马铃薯中的愈伤组织积累，我们在其中观察到大量的愈伤组织沉积和病毒无法传播。在PVYO和PVYN菌株之间不同的HCPro C-末端区域内的8个氨基酸残基的取代，并且先前显示是引起HR应答的原因，足以恢复HCPro（O）抑制胼胝质积累的能力，尽管存在抗性宿主背景，与致病性中的新病毒功能一致。
Potato virus Y (PVY; Potyviridae) is a continuing challenge for potato production owing to the increasing popularity of strain-specific resistant cultivars. Hypersensitive resistance (HR) is one type of plant defense responses to restrict virus spread. In many potato cultivars, such as cultivar Premier Russet (PR), local necrosis at the site of infection protects against the most common PVYO strain, but the HR often fails to restrain necrotic strains, which spread systemically. Here, we established the role of callose accumulation in the strain-specific resistance responses to PVY infection. We first uncovered that PVY, independent of the strain, is naturally capable of suppressing pathogenesis-related callose formation in a susceptible host. Such activity can be dissociated from viral replication by the transient expression of the viral-encoded helper component proteinase (HCPro) protein, identifying it as the pathogen elicitor. However, unlike the necrotic strain, PVYO and its corresponding HCPro are unable to block callose accumulation in resistant PR potatoes, in which we observed an abundance of callose deposition and the inability of the virus to spread. The substitution of eight amino acid residues within the HCPro C-terminal region that differ between PVYO and PVYN strains and were previously shown to be responsible for eliciting the HR response, are sufficient to restore the ability of HCPro(O) to suppress callose accumulation, despite the resistant host background, in line with a new viral function in pathogenicity.