Induction of necrosis symptoms by potato virus X in AGO2-silenced tomato plants associates with reduced transcript accumulation of copper chaperon for superoxide dismutase gene

IF 2.5 4区 医学 Q3 VIROLOGY
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Abstract

RNA silencing is a prominent antiviral defense mechanism in plants. When infected with a virus, RNA silencing–deficient plants tend to show exacerbated symptoms along with increased virus accumulation. However, how symptoms are exacerbated is little understood. Here, we investigated the role of the copper chaperon for superoxide dismutase (CCS) 1, in systemic necrosis observed in Argonaute (AGO)2-silenced tomato plants infected with potato virus X (PVX). While infection with the UK3 strain of PVX induced mosaic symptoms in tomato plants, systemic necrosis occurred when AGO2 was silenced. The CCS1 mRNA level was reduced and micro RNA398 (miR398), which potentially target CCS1, was increased in AGO2-knockdown tomato plants infected with PVX-UK3. Ectopic expression of CCS1 using recombinant PVX attenuated necrosis, suggesting that CCS1 alleviates systemic necrosis by activating superoxide dismutases to scavenge reactive oxygen species. Previous reports have indicated a decrease in the levels of CCS1 and superoxide dismutases along with an increased level of miR398 in plants infected with other viruses and viroids, and thus might represent shared regulatory mechanisms that exacerbate symptoms in these plants.

马铃薯病毒 X 对 AGO2 沉默的番茄植株坏死症状的诱导与超氧化物歧化酶铜伴侣基因转录本积累减少有关。
RNA 沉默是植物中一种重要的抗病毒防御机制。当感染病毒时,RNA 沉默缺陷植物往往会表现出症状加重和病毒积累增加的现象。然而,人们对症状是如何加剧的却知之甚少。在此,我们研究了超氧化物歧化酶铜伴侣(CCS)1在Argonaute(AGO)2沉默的番茄植株感染马铃薯病毒X(PVX)后出现的系统性坏死中的作用。感染了 PVX UK3 株系的番茄植株会出现马赛克症状,而当 AGO2 被沉默时,则会出现系统性坏死。在感染 PVX-UK3 的 AGO2 基因敲除番茄植株中,CCS1 mRNA 水平降低,可能靶向 CCS1 的微 RNA398(miR398)水平升高。利用重组 PVX 异位表达 CCS1 可减轻坏死,这表明 CCS1 可通过激活超氧化物歧化酶清除活性氧来减轻系统性坏死。以前的报告表明,在感染其他病毒和病毒病的植物中,CCS1 和超氧化物歧化酶的水平会降低,同时 miR398 的水平也会升高,因此这可能是加剧这些植物症状的共同调控机制。
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来源期刊
Virus research
Virus research 医学-病毒学
CiteScore
9.50
自引率
2.00%
发文量
239
审稿时长
43 days
期刊介绍: Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.
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