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水杨酸介导的柑橘对不同频率的取食和病原体接种的免疫反应。

Salicylic acid mediated immune response of Citrus sinensis to varying frequencies of herbivory and pathogen inoculation.

机构信息

Department of Entomology and Nematology, Citrus Research and Education Center, University of Florida, Lake Alfred, Florida, 33850, USA.

Present address: Texas A&M University-AgriLife Research, 2415 E Highway 83 -, Weslaco, TX, 78596, USA.

出版信息

BMC Plant Biol. 2022 Jan 3;22(1):7. doi: 10.1186/s12870-021-03389-5.

DOI:10.1186/s12870-021-03389-5
PMID:34979915
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8722004/
Abstract

BACKGROUND

Plant immunity against pathogens and pests is comprised of complex mechanisms orchestrated by signaling pathways regulated by plant hormones [Salicylic acid (SA) and Jasmonic acid (JA)]. Investigations of plant immune response to phytopathogens and phloem-feeders have revealed that SA plays a critical role in reprogramming of the activity and/or localization of transcriptional regulators via post-translational modifications. We explored the contributing effects of herbivory by a phytopathogen vector [Asian citrus psyllid, Diaphorina citri] and pathogen [Candidatus Liberibacter asiaticus (CaLas)] infection on response of sweet orange [Citrus sinensis (L.) Osbeck] using manipulative treatments designed to mimic the types of infestations/infections that citrus growers experience when cultivating citrus in the face of Huanglongbing (HLB) disease.

RESULTS

A one-time (7 days) inoculation access period with CaLas-infected vectors caused SA-associated upregulation of PR-1, stimulating defense response after a long period of infection without herbivory (270 and 360 days). In contrast, while repeated (monthly) 'pulses' of 7 day feeding injury by psyllids stimulated immunity in CaLas-infected citrus by increasing SA in leaves initially (up to 120 days), long-term (270 and 360 days) repeated herbivory caused SA to decrease coincident with upregulation of genes associated with SA metabolism (BMST and DMR6). Similarly, transcriptional responses and metabolite (SA and its analytes) accumulation in citrus leaves exposed to a continuously reproducing population of D. citri exhibited a transitory upregulation of genes associated with SA signaling at 120 days and a posterior downregulation after long-term psyllid (adults and nymphs) feeding (270 and 360 days).

CONCLUSIONS

Herbivory played an important role in regulation of SA accumulation in mature leaves of C. sinensis, whether or not those trees were coincidentally infected with CaLas. Our results indicate that prevention of feeding injury inflicted by D. citri from the tritrophic interaction may allow citrus plants to better cope with the consequences of CaLas infection, highlighting the importance of vector suppression as a component of managing this cosmopolitan disease.

摘要

背景

植物对病原体和害虫的免疫由植物激素(水杨酸(SA)和茉莉酸(JA))调控的信号通路组成的复杂机制组成。对植物免疫反应的研究表明,植物对植物病原体和韧皮部取食者的反应,SA 通过翻译后修饰在转录调控因子的活性和/或定位的重编程中起关键作用。我们通过操纵处理探索了植物病原体载体(亚洲柑橘木虱,Diaphorina citri)和病原体(柑橘黄龙病菌(CaLas))感染对甜橙[Citrus sinensis(L.)Osbeck]的影响,这些处理旨在模拟柑橘种植者在面对黄龙病(HLB)时种植柑橘时所经历的侵染/感染类型。

结果

一次(7 天)接种感染期的 CaLas 感染载体导致 SA 相关的 PR-1 上调,在没有取食(270 和 360 天)的长时间感染后刺激防御反应。相比之下,虽然每月通过木虱进行 7 天的“脉冲”取食伤害刺激了 CaLas 感染柑橘的免疫,最初增加了叶片中的 SA(长达 120 天),但长期(270 和 360 天)重复取食导致 SA 下降,同时与 SA 代谢(BMST 和 DMR6)相关的基因上调。同样,暴露于不断繁殖的 D. citri 种群的柑橘叶片中的转录反应和代谢物(SA 及其分析物)积累在 120 天时表现出与 SA 信号相关的基因的短暂上调,并且在长期木虱(成虫和若虫)取食(270 和 360 天时)后下调。

结论

取食伤害在调节甜橙成熟叶片中的 SA 积累方面起着重要作用,无论这些树是否碰巧感染了 CaLas。我们的结果表明,从三营养体相互作用中防止 D. citri 的取食伤害可能使柑橘植物更好地应对 CaLas 感染的后果,突出了作为管理这种世界性疾病的一部分抑制媒介的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/e0a5e70ab9c4/12870_2021_3389_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/501078e3afd7/12870_2021_3389_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/5185cdcd5944/12870_2021_3389_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/b09a6ab559e2/12870_2021_3389_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/e0a5e70ab9c4/12870_2021_3389_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/501078e3afd7/12870_2021_3389_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/5185cdcd5944/12870_2021_3389_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/b09a6ab559e2/12870_2021_3389_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d55/8722004/e0a5e70ab9c4/12870_2021_3389_Fig4_HTML.jpg

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