Rivera-Zuluaga Katherine, Choudhary Pratibha, Mohammad Sana, Caldwell Denise, Leuschen-Kohl Rebecca, Pascuzzi Pete E, Iyer-Pascuzzi Anjali
Department of Botany and Plant Pathology and Center for Plant Biology, Purdue University, West Lafayette, IN 47907, U.S.A.
Purdue University Libraries and School of Information Studies, West Lafayette, IN 47907, U.S.A.
Mol Plant Microbe Interact. 2025 Jul;38(4):566-578. doi: 10.1094/MPMI-10-24-0123-R. Epub 2025 Aug 11.
Quantitative disease resistance (QDR) is the most common form of disease resistance in crops, but it is challenging to understand at the cellular level due to the involvement of many genes and biological processes. , the causal agent of bacterial wilt disease, is a destructive plant pathogen of Solanaceous species that is best controlled by quantitatively resistant varieties, but few QDR genes are known. We previously found that a tomato auxin pathway mutant known as () has enhanced resistance to . Here, we show that, as with wild-type quantitatively resistant tomato plants, resistance in is the result of multiple mechanisms. Mock-inoculated roots have endogenously higher levels of the plant defense hormone salicylic acid (SA). However, the SA-deficient double mutant is still resistant to , indicating that SA-independent pathways are also required for resistance. Scanning electron microscopy revealed that colonization of the root xylem is delayed in . We found an increased number of lignified xylem cells and altered root vasculature anatomy in , and root length was not impacted by treatment. Similar to the wilt-resistant wild-type tomato Hawaii7996, RNA sequencing results suggested that may tolerate -induced water stress better than the wilt-susceptible parent. Thus, resistance in is due to several pathways, including preactivated SA defenses, physical barriers in the xylem, and an ability to tolerate water stress. The pleiotropic nature of this single mutation appears to mimic quantitative resistance. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
数量抗病性（QDR）是作物中最常见的抗病形式，但由于涉及许多基因和生物过程，在细胞水平上理解它具有挑战性。青枯雷尔氏菌是细菌性枯萎病的病原体，是茄科植物的一种毁灭性植物病原体，最好通过数量抗性品种进行控制，但已知的QDR基因很少。我们之前发现，一种名为（）的番茄生长素途径突变体对青枯雷尔氏菌的抗性增强。在这里，我们表明，与野生型数量抗性番茄植株一样，（突变体）的抗性是多种机制的结果。模拟接种的（突变体）根系内源性地具有较高水平的植物防御激素水杨酸（SA）。然而，缺乏SA的双突变体（）仍然对青枯雷尔氏菌具有抗性，这表明抗性也需要SA非依赖途径。扫描电子显微镜显示，青枯雷尔氏菌在（突变体）根木质部的定殖延迟。我们发现（突变体）中木质化的木质部细胞数量增加，根维管系统解剖结构改变，并且（突变体）根的长度不受青枯雷尔氏菌处理的影响。与抗枯萎病的野生型番茄品种夏威夷7996类似，RNA测序结果表明，（突变体）可能比易感枯萎病的亲本更能耐受青枯雷尔氏菌诱导的水分胁迫。因此，（突变体）的抗性归因于多种途径，包括预激活的SA防御、木质部中的物理屏障以及耐受水分胁迫的能力。这种单一突变的多效性似乎模拟了数量抗性。[公式：见正文] 版权所有©2025作者。这是一篇根据知识共享署名 - 非商业性使用 - 禁止演绎4.0国际许可协议分发的开放获取文章。
