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冷敏在拟南芥突变体背景下对病原体易感性的影响需要一个功能的 。

Cold priming on pathogen susceptibility in the Arabidopsis mutant background requires a functional .

机构信息

Plant Physiology, Dahlem Centre of Plant Sciences, Freie Universität Berlin, Berlin, Germany.

出版信息

Plant Signal Behav. 2024 Dec 31;19(1):2300239. doi: 10.1080/15592324.2023.2300239. Epub 2024 Jan 3.

DOI:10.1080/15592324.2023.2300239
PMID:38170666
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10766390/
Abstract

24 h cold exposure (4°C) is sufficient to reduce pathogen susceptibility in against the virulent pv. () strain even when the infection occurs five days later. This priming effect is independent of the immune regulator Enhanced Disease Susceptibility 1 (EDS1) and can be observed in the immune-compromised null mutant. In contrast, cold priming-reduced susceptibility is strongly impaired in knock-out lines of the stromal and thylakoid ascorbate peroxidases (sAPX/tAPX) highlighting their relevance for abiotic stress-related increased immune resilience. Here, we extended our analysis by generating an double mutant. showed -like resistance and susceptibility phenotypes against strains containing the effectors avrRPM1 and avrRPS4. In comparison to , susceptibility against the wildtype strain was constitutively enhanced in . Although a prior cold priming exposure resulted in reduced titers in , it did not alter resistance in . This demonstrates that the genetic requirement for cold priming of basal plant immunity applies also to an null mutant background.

摘要

24 小时的冷暴露(4°C)足以降低 对强毒 pv. ()菌株的病原体易感性,即使感染发生在五天后。这种启动效应独立于免疫调节剂增强疾病易感性 1(EDS1),并且可以在免疫缺陷的 缺失突变体中观察到。相比之下,冷启动降低的 易感性在基质和类囊体抗坏血酸过氧化物酶(sAPX/tAPX)的敲除系中受到严重损害,这突出了它们在与非生物胁迫相关的增强免疫弹性方面的相关性。在这里,我们通过生成一个 双突变体来扩展我们的分析。 表现出对含有效应物 avrRPM1 和 avrRPS4 的 菌株的类似抗性和易感性表型。与 相比, 在野生型 菌株中的易感性被持续增强。尽管先前的冷暴露会导致 的滴度降低,但它并没有改变 在 中的抗性。这表明,基础植物免疫的冷启动的遗传 要求也适用于 缺失突变体背景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9906/10766390/52b085cb353c/KPSB_A_2300239_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9906/10766390/03b910267e61/KPSB_A_2300239_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9906/10766390/52b085cb353c/KPSB_A_2300239_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9906/10766390/03b910267e61/KPSB_A_2300239_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9906/10766390/52b085cb353c/KPSB_A_2300239_F0002_OC.jpg

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Chemical priming of plant defense responses to pathogen attacks.植物对病原体攻击的防御反应的化学引发
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Light prevents pathogen-induced aqueous microenvironments via potentiation of salicylic acid signaling.光照通过增强水杨酸信号来阻止病原体诱导的水样微环境。
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Ascorbate peroxidase postcold regulation of chloroplast NADPH dehydrogenase activity controls cold memory.抗坏血酸过氧化物酶后冷调节叶绿体 NADPH 脱氢酶活性控制冷记忆。
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TIR-catalyzed ADP-ribosylation reactions produce signaling molecules for plant immunity.TIR 催化的 ADP-ribosylation 反应产生植物免疫的信号分子。
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Chloroplastic ascorbate peroxidases targeted to stroma or thylakoid membrane: The chicken or egg dilemma.靶向基质或类囊体膜的叶绿体抗坏血酸过氧化物酶:先有鸡还是先有蛋的困境。
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