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Stagonospora nodorum 和 Pyrenophora tritici-repentis 中 ToxA 同工型效应物活性的定量变异。

Quantitative variation in effector activity of ToxA isoforms from Stagonospora nodorum and Pyrenophora tritici-repentis.

机构信息

Environment and Agriculture, Curtin University, Bentley WA 6102, Australia.

出版信息

Mol Plant Microbe Interact. 2012 Apr;25(4):515-22. doi: 10.1094/MPMI-10-11-0273.

DOI:10.1094/MPMI-10-11-0273
PMID:22250581
Abstract

ToxA is a proteinaceous necrotrophic effector produced by Stagonospora nodorum and Pyrenophora tritici-repentis. In this study, all eight mature isoforms of the ToxA protein were purified and compared. Circular dichroism spectra indicated that all isoforms were structurally intact and had indistinguishable secondary structural features. ToxA isoforms were infiltrated into wheat lines that carry the sensitivity gene Tsn1. It was observed that different wheat lines carrying identical Tsn1 alleles varied in sensitivity to ToxA. All ToxA isoforms induced necrosis when introduced into any Tsn1 wheat line but we observed quantitative variation in effector activity, with the least-active version found in isolates of P. tritici-repentis. Pathogen sporulation increased with higher doses of ToxA. The isoforms that induced the most rapid necrosis also induced the most sporulation, indicating that pathogen fitness is affected by differences in ToxA activity. We show that differences in toxin activity encoded by a single gene can contribute to the quantitative inheritance of necrotrophic virulence. Our findings support the hypothesis that the variation at ToxA results from selection that favors increased toxin activity.

摘要

ToxA 是由 Stagonospora nodorum 和 Pyrenophora tritici-repentis 产生的蛋白性坏死效应物。在这项研究中,对 ToxA 蛋白的所有 8 种成熟同工型进行了纯化和比较。圆二色光谱表明,所有同工型结构完整,具有相似的二级结构特征。ToxA 同工型被注入携带敏感性基因 Tsn1 的小麦品系中。观察到携带相同 Tsn1 等位基因的不同小麦品系对 ToxA 的敏感性存在差异。所有 ToxA 同工型在引入任何 Tsn1 小麦品系时都会诱导坏死,但我们观察到效应物活性存在定量变化,活性最低的版本存在于 P. tritici-repentis 的分离物中。病原体孢子形成随着 ToxA 剂量的增加而增加。诱导最快坏死的同工型也诱导最多的孢子形成,表明病原体适应性受到 ToxA 活性差异的影响。我们表明,单个基因编码的毒素活性差异可导致坏死毒力的定量遗传。我们的研究结果支持这样一种假设,即 ToxA 的变异是由增加毒素活性的选择所导致的。

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