• Necrosis- and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) constitute a superfamily of proteins toxic to dicot plants, but the molecular basis of this toxicity remains obscure.
• Using quantitative trait locus (QTL) analysis we investigated the genetic variation underlying ion leakage in Arabidopsis plants elicited with MoNLP1 derived from Magnaporthe oryzae. The QTL conditioning MoNLP1 toxicity was positionally cloned and further characterized to elucidate its mode of action.
• MoNLP1-triggered cell death varied significantly across > 250 Arabidopsis accessions and three QTLs were identified conferring the observed variation. The QTL on chromosome 4 was uncovered to encode a leucine-rich repeat (LRR)-only protein designated as NTCD4, which shares high sequence identity with a set of nucleotide-binding LRR proteins. NTCD4 was secreted into the apoplast and physically interacted with multiple NLPs. Apoplastic NTCD4 facilitated the oligomerization of NLP, which was closely associated with toxicity in planta. The natural genetic variation causing D3N change in NTCD4 reduced the secretion efficiency of NTCD4 and the infection of Botrytis cinerea on Arabidopsis plants.
• These observations demonstrate that the plant-derived NTCD4 is recruited by NLPs to promote toxicity via facilitating their oligomerization, which extends our understanding of a key step in the toxic mode of action of NLPs.

中文翻译：

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仅 LRR 的蛋白质通过促进拟南芥中 NLP 的寡聚化来促进 NLP 触发的细胞死亡和疾病易感性

• 坏死和乙烯诱导肽 1 (Nep1) 样蛋白 (NLP) 构成对双子叶植物有毒的蛋白质超家族，但这种毒性的分子基础仍不清楚。
• 使用数量性状基因座 (QTL) 分析，我们研究了拟南芥植物中离子泄漏的遗传变异，这些变异是由来自稻瘟病菌的MoNLP1 引起的。对调节 MoNLP1 毒性的 QTL 进行定位克隆并进一步表征以阐明其作用模式。
• MoNLP1 触发的细胞死亡在 > 250 个拟南芥种质中差异显着，并且确定了三个 QTL，赋予观察到的变异。发现第 4 号染色体上的 QTL 编码一个富含亮氨酸重复序列 (LRR) 的蛋白质，称为 NTCD4，它与一组核苷酸结合 LRR 蛋白质具有高度的序列同一性。NTCD4 被分泌到质外体中，并与多个 NLP 发生物理相互作用。质外体 NTCD4 促进了 NLP 的寡聚化，这与植物中的毒性密切相关。导致 NTCD4 D3N 变化的自然遗传变异降低了 NTCD4 的分泌效率和灰葡萄孢对拟南芥植物的感染。
• 这些观察结果表明，植物来源的 NTCD4 被 NLP 募集以通过促进它们的寡聚化来促进毒性，这扩展了我们对 NLP 毒性作用模式的关键步骤的理解。