Genome analyses of the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici reveal polymorphic and haustorial expressed secreted proteins as candidate effectors.
Genome analyses of the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici reveal polymorphic and haustorial expressed secreted proteins as candidate effectors.
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DOI：
10.1186/1471-2164-14-270
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发表时间：
2013-04-22
期刊：
影响因子：
4.4
通讯作者：
Uauy C
中科院分区：
文献类型：
--
作者：
Cantu D;Segovia V;MacLean D;Bayles R;Chen X;Kamoun S;Dubcovsky J;Saunders DG;Uauy C
小麦条锈病是由条锈菌（Pucciniastriiformis f.）小麦赤霉病（PST）是世界范围内小麦最具毁灭性的病害之一。为了设计有效的育种策略，最大限度地提高持久抗病性的潜力，重要的是要了解PST致病性的分子基础。特别是，由宿主免疫受体检测的分泌的效应蛋白的结构、功能和进化动力学的表征可以帮助指导和优先考虑育种工作。然而，迄今为止，我们的知识的效应库的谷物锈病病原体是有限的。我们对来自美国和英国的四种PST分离株的基因组进行了重新测序，以确定效应候选物，并将其与其不同的毒力谱联系起来。首先，我们评估了所有分离株之间的SNP频率，异源SNP的频率（5.29 ± 2.23 SNP/kb）是同核SNP（0.41 ± 0.28 SNP/kb）的十倍以上。接下来，我们实施了一个生物信息学管道，以整合基因组学，转录组学和以效应子为中心的注释，以识别和分类PST中的效应子候选者。RNAseq分析突出了编码分泌蛋白的转录物，与感染的组织相比，所述分泌蛋白在吸器中显著富集。使用qRT-PCR表征了22个候选效应基因的表达，揭示了小麦感染期间不同的时间表达模式。最后，我们确定了两个英国分离株PST-87/7和PST-08/21之间特异性显示非同义取代的蛋白质，这两个分离株对两个小麦品种的毒性不同。通过关注吸器中富集的多态性变体，我们在2，999个分泌蛋白中鉴定了PST-87/7和PST-08/21之间的5个多态性效应子候选物。这些等位基因变体现在是在相应的小麦品种中作为毒力/无毒力效应子进行功能验证的优先考虑。整合基因组学，转录组学，和效应器导向的注释的PST分离株，使我们能够超越单一的分离株导向的目录的效应蛋白，并开发一个框架，挖掘效应蛋白在密切相关的分离株，并将这些回他们定义的毒力档案。这将最终导致对PST致病系统的更全面的理解，这是为小麦最具破坏性的病原体之一制定更有效的监测和管理策略的重要的第一步。
Wheat yellow (stripe) rust caused by Puccinia striiformis f. sp. tritici (PST) is one of the most devastating diseases of wheat worldwide. To design effective breeding strategies that maximize the potential for durable disease resistance it is important to understand the molecular basis of PST pathogenicity. In particular, the characterisation of the structure, function and evolutionary dynamics of secreted effector proteins that are detected by host immune receptors can help guide and prioritize breeding efforts. However, to date, our knowledge of the effector repertoire of cereal rust pathogens is limited. We re-sequenced genomes of four PST isolates from the US and UK to identify effector candidates and relate them to their distinct virulence profiles. First, we assessed SNP frequencies between all isolates, with heterokaryotic SNPs being over tenfold more frequent (5.29 ± 2.23 SNPs/kb) than homokaryotic SNPs (0.41 ± 0.28 SNPs/kb). Next, we implemented a bioinformatics pipeline to integrate genomics, transcriptomics, and effector-focused annotations to identify and classify effector candidates in PST. RNAseq analysis highlighted transcripts encoding secreted proteins that were significantly enriched in haustoria compared to infected tissue. The expression of 22 candidate effector genes was characterised using qRT-PCR, revealing distinct temporal expression patterns during infection in wheat. Lastly, we identified proteins that displayed non-synonymous substitutions specifically between the two UK isolates PST-87/7 and PST-08/21, which differ in virulence to two wheat varieties. By focusing on polymorphic variants enriched in haustoria, we identified five polymorphic effector candidates between PST-87/7 and PST-08/21 among 2,999 secreted proteins. These allelic variants are now a priority for functional validation as virulence/avirulence effectors in the corresponding wheat varieties. Integration of genomics, transcriptomics, and effector-directed annotation of PST isolates has enabled us to move beyond the single isolate-directed catalogues of effector proteins and develop a framework for mining effector proteins in closely related isolates and relate these back to their defined virulence profiles. This should ultimately lead to more comprehensive understanding of the PST pathogenesis system, an important first step towards developing more effective surveillance and management strategies for one of the most devastating pathogens of wheat.