The soybean cyst nematode (SCN) is one of the most important causes of soybean yield loss. The major source of genetic resistance to SCN is the Rhg1 repeat, a tandem copy number polymorphism of three genes. The roles of these genes are only partially understood. Moreover, nematode populations virulent on Rhg1-carrying soybeans are becoming more common, increasing the need to understand the most successful genetic resistance mechanism. Here, we show that a Rhg1-locus gene (Glyma.18G02270) encoding a wound-inducible protein (WI12_Rhg1) is needed for SCN resistance. Furthermore, knockout of WI12_Rhg1 reduces the expression of DELLA18, and the expression of WI12_Rhg1 is itself induced by either JA, SA or GA. The content of the defence hormone SA is significantly lower whilst GA₁₂ and GA₅₃ are increased in WI12_Rhg1 knockout roots compared with unedited hairy roots. We find that WI12_Rhg1 directly interacts with DELLA18 (Glyma.18G040000) in yeast and plants and that double knockout of DELLA18 and its homeolog DELLA11 (Glyma.11G216500) significantly reduces SCN resistance and alters the root morphology. As DELLA proteins are implicated in hormone signalling, we explored the content of defence hormones (JA and SA) in DELLA knockout and unedited roots, finding reduced levels of JA and SA after the knockout of DELLA. Additionally, the treatment of DELLA-knockout roots with JA or SA rescues SCN resistance lost by the knockout. Meanwhile, the SCN resistance of unedited roots decreases after the treatment with GA, but increases with JA or SA. Our findings highlight the critical roles of WI12_Rhg1 and DELLA proteins in SCN resistance through interconnection with hormone signalling.

中文翻译：

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WI12Rhg1 与 DELLA 相互作用并通过激素途径介导大豆胞囊线虫抗性


大豆胞囊线虫(SCN)是导致大豆减产的最重要原因之一。 SCN 遗传抗性的主要来源是Rhg1重复序列，即三个基因的串联拷贝数多态性。这些基因的作用仅被部分了解。此外，对携带Rhg1的大豆具有毒性的线虫种群正变得越来越普遍，这增加了了解最成功的遗传抗性机制的必要性。在这里，我们表明编码伤口诱导蛋白（WI12 _Rhg1 ）的Rhg1位点基因（Glyma.18G02270）是SCN抗性所必需的。此外，敲除WI12 _Rhg1会降低DELLA18的表达，并且WI12 _Rhg1的表达本身是由JA、SA或GA诱导的。与未编辑的毛状根相比， WI12 _Rhg1敲除根中防御激素 SA 的含量显着降低，而 GA ₁₂和 GA ₅₃增加。我们发现 WI12 _Rhg1直接与酵母和植物中的 DELLA18 (Glyma.18G040000) 相互作用，并且双敲除DELLA18及其同源物DELLA11 (Glyma.11G216500) 显着降低 SCN 抗性并改变根形态。由于 DELLA 蛋白与激素信号传导有关，我们探索了DELLA敲除和未编辑的根中防御激素（JA 和 SA）的含量，发现DELLA敲除后 JA 和 SA 的水平降低。此外，用JA或SA处理DELLA敲除的根可挽救因敲除而丧失的SCN抗性。 同时，未编辑根的SCN抗性在GA处理后降低，但在JA或SA处理后增加。我们的研究结果强调了 WI12 _Rhg1和 DELLA 蛋白通过与激素信号传导互连在 SCN 抵抗中的关键作用。