Tomato is one of the most popular horticultural crops, and many commercial tomato cultivars are particularly susceptible to Botrytis cinerea. Nonexpressor of pathogenesis-related gene 1 (NPR1) is a critical component of plant defense mechanism. However, our understanding of how SlNPR1 influences disease resistance in tomato is still limited. In this study, two independent slnpr1 mutants were used to study the role of SlNPR1 in tomato resistance against B. cinerea. Compared to WT, slnpr1 leaves exhibited enhanced resistance against B. cinerea with smaller lesion sizes, higher activities of chitinase (CHI), β-1, 3-glucanases (GLU), and phenylalanine ammonia-lyase (PAL), and significantly increased expressions of pathogenesis-related genes (PRs). The increased activities of peroxidase (POD), ascorbate peroxidase (APX) and decreased catalase (CAT) activities collectively regulated reactive oxygen species (ROS) homeostasis in slnpr1 mutants. The integrity of the cell wall in slnpr1 mutants was maintained. Moreover, the enhanced resistance was further reflected by induction of defense genes involved in jasmonic acid (JA) and ethylene (ET) signaling pathways. Taken together, these findings revealed that knockout of SlNPR1 resulted in increased activities of defense enzymes, changes in ROS homeostasis and integrity of cell walls, and activation of JA and ET pathways, which confers resistance against B. cinerea in tomato plants. This article is protected by copyright. All rights reserved.

中文翻译：

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敲除 SlNPR1 通过调节 ROS 稳态和 JA/ET 信号通路增强番茄植株对灰霉病菌的抗性

番茄是最受欢迎的园艺作物之一，许多商业番茄品种特别容易感染灰霉病菌。发病机制相关基因1（NPR1）的非表达基因是植物防御机制的重要组成部分。然而，我们对 SlNPR1 如何影响番茄抗病性的理解仍然有限。在这项研究中，两个独立的 slnpr1 突变体被用来研究 SlNPR1 在番茄抗 B. cinerea 中的作用。与 WT 相比，slnpr1 叶片对 B. cinerea 的抗性增强，病斑较小，几丁质酶 (CHI)、β-1, 3-葡聚糖酶 (GLU) 和苯丙氨酸解氨酶 (PAL) 活性较高，表达量显着增加发病机制相关基因（PRs）。过氧化物酶（POD）的活性增加，抗坏血酸过氧化物酶 (APX) 和过氧化氢酶 (CAT) 活性降低共同调节 slnpr1 突变体中的活性氧 (ROS) 稳态。slnpr1 突变体中细胞壁的完整性得以保持。此外，通过诱导参与茉莉酸（JA）和乙烯（ET）信号通路的防御基因进一步反映了增强的抗性。总之，这些发现表明，敲除 SlNPR1 导致防御酶活性增加，ROS 稳态和细胞壁完整性的变化，以及 JA 和 ET 途径的激活，从而赋予番茄植物对灰霉病菌的抗性。本文受版权保护。版权所有。此外，通过诱导参与茉莉酸（JA）和乙烯（ET）信号通路的防御基因进一步反映了增强的抗性。总之，这些发现表明，敲除 SlNPR1 导致防御酶活性增加，ROS 稳态和细胞壁完整性的变化，以及 JA 和 ET 途径的激活，从而赋予番茄植物对灰霉病菌的抗性。本文受版权保护。版权所有。此外，通过诱导参与茉莉酸（JA）和乙烯（ET）信号通路的防御基因进一步反映了增强的抗性。总之，这些发现表明，敲除 SlNPR1 导致防御酶活性增加，ROS 稳态和细胞壁完整性的变化，以及 JA 和 ET 途径的激活，从而赋予番茄植物对灰霉病菌的抗性。本文受版权保护。版权所有。赋予番茄植物对灰霉病菌的抗性。本文受版权保护。版权所有。赋予番茄植物对灰霉病菌的抗性。本文受版权保护。版权所有。