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根结线虫早期感染抑制番茄的免疫反应并引发其抗氧化系统。

Root-Knot Nematode Early Infection Suppresses Immune Response and Elicits the Antioxidant System in Tomato.

作者信息

Molinari Sergio, Farano Anna Carla, Leonetti Paola

机构信息

Bari Unit, Institute for Sustainable Plant Protection, Department of Biology, Agricultural and Food Sciences, National Research Council of Italy, 70126 Bari, Italy.

Sant'Anna School of Advanced Studies, 56127 Pisa, Italy.

出版信息

Int J Mol Sci. 2024 Nov 23;25(23):12602. doi: 10.3390/ijms252312602.

DOI:10.3390/ijms252312602
PMID:39684315
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11641414/
Abstract

The immune response in plants is regulated by several phytohormones and involves the overexpression of defense genes, including the pathogenesis-related () genes. The data reported in this paper indicate that nematodes can suppress the immune response by inhibiting the expression of defense genes. Transcripts from nine defense genes were detected by qRT-PCR in the roots of tomato plants at three and seven days post-inoculation (dpi) with living juveniles (J2s) of (root-knot nematodes, RKNs). All the salicylic acid (SA)-responsive genes tested (, , , ) were down-regulated in response to nematode infection. On the contrary, the expression of jasmonic acid (JA)-responsive genes, including (encoding the enzyme 1-aminocyclopropane-1-carboxylic acid oxidase, which catalyzes the last step of ethylene (ET) biosynthesis) and (), was unaffected by the infection. Conversely, the effect of nematode attack on the activities of the defense enzymes endoglucanase and endochitinase, encoded by and respectively, changed depending on the tested dpi. At 5 dpi, both enzymes were inhibited in inoculated plants compared to healthy controls. The genes encoding glutathione peroxidase () and catalase (), both part of the antioxidant plant system, were highly overexpressed. Additionally, the activity of the antioxidant enzymes superoxide dismutase (SOD), CAT, and ascorbate peroxidase (APX) was enhanced in infected roots. Isoelectrofocusing of root extracts revealed novel SOD isoforms in samples from inoculated plants. Furthermore, plants were pre-treated with an array of key compounds, including hormone generators, inhibitors of SA or JA-mediated defense pathways, reactive oxygen species (ROS) scavengers and generators, inhibitors of ROS generation, and compounds that interfere with calcium-mediated metabolism. After treatments, plants were inoculated with RKNs, and nematodes were allowed to complete their life cycle. Factors of plant growth and infection level in treated plants were compared with those from untreated inoculated plants. Generally, compounds that decreased SA and/or ROS levels increased infection severity, while those that reduced JA/ET levels did not affect infection rates. ROS generators induced resistance against the pests. Compounds that silence calcium signaling by preventing its intake augmented infection symptoms. The data shown in this paper indicate that SA-mediated plant immune responses are consistently suppressed during the early stages of nematode infection, and this restriction is associated with the activation of the antioxidant ROS-scavenging system.

摘要

植物中的免疫反应受多种植物激素调节,涉及防御基因的过表达,包括病程相关(PR)基因。本文报道的数据表明,线虫可通过抑制防御基因的表达来抑制免疫反应。在接种南方根结线虫(RKN)活幼虫(J2)后3天和7天,通过qRT-PCR检测番茄植株根中9个防御基因的转录本。所有测试的水杨酸(SA)响应基因(PR1、PR2、PR5、PR10)在受到线虫感染后均下调。相反,茉莉酸(JA)响应基因的表达,包括ACO1(编码催化乙烯(ET)生物合成最后一步的1-氨基环丙烷-1-羧酸氧化酶)和PDF1.2,不受感染影响。相反,线虫攻击对分别由PR-endo和PR-chit编码的防御酶内切葡聚糖酶和内切几丁质酶活性的影响,取决于测试的接种后天数(dpi)。在5 dpi时,与健康对照相比,接种植物中的这两种酶均受到抑制。编码谷胱甘肽过氧化物酶(GPX)和过氧化氢酶(CAT)的基因,均为植物抗氧化系统的一部分,高度过表达。此外,感染根中抗氧化酶超氧化物歧化酶(SOD)、CAT和抗坏血酸过氧化物酶(APX)的活性增强。根提取物的等电聚焦显示接种植物样品中有新的SOD同工型。此外,用一系列关键化合物对植物进行预处理,包括激素生成剂、SA或JA介导的防御途径抑制剂、活性氧(ROS)清除剂和生成剂、ROS生成抑制剂以及干扰钙介导代谢的化合物。处理后,用RKN接种植物,并让线虫完成其生命周期。将处理过的植物中的植物生长和感染水平因素与未处理的接种植物进行比较。一般来说,降低SA和/或ROS水平的化合物会增加感染严重程度,而降低JA/ET水平的化合物不会影响感染率。ROS生成剂诱导对害虫的抗性。通过阻止钙摄入使钙信号沉默的化合物会加剧感染症状。本文所示数据表明,在 nematode感染的早期阶段,SA介导的植物免疫反应持续受到抑制,这种限制与抗氧化ROS清除系统的激活有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/7d95eb33750f/ijms-25-12602-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/061635166b53/ijms-25-12602-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/7d95eb33750f/ijms-25-12602-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/061635166b53/ijms-25-12602-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/60c218e900c8/ijms-25-12602-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/8b78d1214cb0/ijms-25-12602-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/d3f295464587/ijms-25-12602-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5645/11641414/7d95eb33750f/ijms-25-12602-g005.jpg

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