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Correction to Cassava molecular genetics and genomics for enhanced resistance to diseases and pests. 更正木薯分子遗传学和基因组学,以增强对病虫害的抵抗力。
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-02-01 DOI: 10.1111/mpp.13432
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引用次数: 0
Turnip mosaic virus NIb weakens the function of eukaryotic translation initiation factor 6 facilitating viral infection in Nicotiana benthamiana. 芜菁花叶病毒 NIb 可削弱真核翻译起始因子 6 的功能,从而促进烟草花叶病毒的感染。
IF 4.8 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-02-01 DOI: 10.1111/mpp.13434
Ziqiang Chen, Feng Wang, Binghua Chen, Guanwei Wu, Dagang Tian, Quan Yuan, Shiyou Qiu, Yushan Zhai, Jianping Chen, Hongying Zheng, Fei Yan

Viruses rely completely on host translational machinery to produce the proteins encoded by their genes. Controlling translation initiation is important for gaining translational advantage in conflicts between the host and virus. The eukaryotic translation initiation factor 4E (eIF4E) has been reported to be hijacked by potyviruses for virus multiplication. The role of translation regulation in defence and anti-defence between plants and viruses is not well understood. We report that the transcript level of eIF6 was markedly increased in turnip mosaic virus (TuMV)-infected Nicotiana benthamiana. TuMV infection was impaired by overexpression of N. benthamiana eIF6 (NbeIF6) either transiently expressed in leaves or stably expressed in transgenic plants. Polysome profile assays showed that overexpression of NbeIF6 caused the accumulation of 40S and 60S ribosomal subunits, the reduction of polysomes, and also compromised TuMV UTR-mediated translation, indicating a defence role for upregulated NbeIF6 during TuMV infection. However, the polysome profile in TuMV-infected leaves was not identical to that in leaves overexpressing NbeIF6. Further analysis showed that TuMV NIb protein, the RNA-dependent RNA polymerase, interacted with NbeIF6 and interfered with its effect on the ribosomal subunits, suggesting that NIb might have a counterdefence role. The results propose a possible regulatory mechanism at the translation level during plant-virus interaction.

病毒完全依赖宿主的翻译机制来产生其基因编码的蛋白质。在宿主与病毒的冲突中,控制翻译起始对于获得翻译优势非常重要。据报道,真核翻译起始因子 4E(eIF4E)被壶状病毒劫持,用于病毒繁殖。翻译调控在植物与病毒之间的防御和反防御中的作用尚不十分清楚。我们报告说,在受芜菁花叶病毒(TuMV)感染的烟草中,eIF6 的转录水平显著增加。在叶片中瞬时表达或在转基因植物中稳定表达的 N. benthamiana eIF6(NbeIF6)的过表达抑制了 TuMV 感染。多聚体图谱分析表明,过表达 NbeIF6 会导致 40S 和 60S 核糖体亚基的积累、多聚体的减少,还会影响 TuMV UTR 介导的翻译,这表明上调的 NbeIF6 在 TuMV 感染过程中起着防御作用。然而,TuMV 感染叶片的多聚体特征与过表达 NbeIF6 的叶片并不相同。进一步分析表明,TuMV NIb 蛋白(RNA 依赖性 RNA 聚合酶)与 NbeIF6 相互作用,干扰了 NbeIF6 对核糖体亚基的影响,这表明 NIb 可能具有反防御作用。研究结果提出了植物与病毒相互作用过程中可能存在的翻译水平调控机制。
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引用次数: 0
Importin α2 participates in RNA interference against bamboo mosaic virus accumulation in Nicotiana benthamiana via NbAGO10a-mediated small RNA clearance 导入蛋白 α2通过 NbAGO10a 介导的小 RNA 清除参与 RNA 干扰,防止竹节病病毒在烟草中积累
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-19 DOI: 10.1111/mpp.13422
Jiun-Da Wang, Yau-Heiu Hsu, Yun-Shien Lee, Na-Sheng Lin
Karyopherins, the nucleocytoplasmic transporters, participate in multiple RNA silencing stages by transporting associated proteins into the nucleus. Importin α is a member of karyopherins and has been reported to facilitate virus infection via nuclear import of viral proteins. Unlike other RNA viruses, silencing of importin α2 (α2i) by virus-induced gene silencing (VIGS) boosted the titre of bamboo mosaic virus (BaMV) in protoplasts, and inoculated and systemic leaves of Nicotiana benthamiana. The enhanced BaMV accumulation in importin α2i plants was linked to reduced levels of RDR6-dependent secondary virus-derived small-interfering RNAs (vsiRNAs). Small RNA-seq revealed importin α2 silencing did not affect the abundance of siRNAs derived from host mRNAs but significantly reduced the 21 and 22 nucleotide vsiRNAs in BaMV-infected plants. Deletion of BaMV TGBp1, an RNA silencing suppressor, compromised importin α2i-mediated BaMV enhancement. Moreover, silencing of importin α2 upregulated NbAGO10a, a proviral protein recruited by TGBp1 for BaMV vsiRNAs clearance, but hindered the nuclear import of NbAGO10a. Taken together, these results indicate that importin α2 acts as a negative regulator of BaMV invasion by controlling the expression and nucleocytoplasmic shuttling of NbAGO10a, which removes vsiRNAs via the TGBp1-NbAGO10a-SDN1 pathway. Our findings reveal the hidden antiviral mechanism of importin α2 in countering BaMV infection in N. benthamiana.
核细胞质转运体 Karyopherins 通过将相关蛋白转运到细胞核中,参与多个 RNA 沉默阶段。导入蛋白α是核糖体蛋白的一种,据报道它通过核导入病毒蛋白来促进病毒感染。与其他 RNA 病毒不同,通过病毒诱导基因沉默(VIGS)沉默导入蛋白 α2(α2i)可提高竹花叶病毒(BaMV)在原生质体、接种叶片和烟草本根叶片中的滴度。导入蛋白α2i植株中BaMV积累的增强与依赖RDR6的次生病毒衍生小干扰RNA(vsiRNA)水平的降低有关。小RNA-seq显示,沉默导入素α2不会影响来自宿主mRNA的siRNA的丰度,但会显著减少BaMV感染植株中21和22个核苷酸的vsiRNA。RNA 沉默抑制因子 BaMV TGBp1 的缺失影响了输入蛋白 α2i介导的 BaMV 增强。此外,沉默导入蛋白α2会上调NbAGO10a,NbAGO10a是TGBp1为清除BaMV vsiRNA而招募的一种病毒蛋白,但会阻碍NbAGO10a的核导入。综上所述,这些结果表明,导入蛋白α2通过控制NbAGO10a的表达和核细胞质穿梭而成为BaMV入侵的负调控因子,而NbAGO10a则通过TGBp1-NbAGO10a-SDN1途径清除vsiRNA。我们的研究结果揭示了导入蛋白α2在抗BaMV感染中的隐性抗病毒机制。
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引用次数: 0
Correction to ‘Different epitopes of Ralstonia solanacearum effector RipAW are recognized by two Nicotiana species and trigger immune responses’ 对 "两种烟草识别 Ralstonia solanacearum 效应子 RipAW 的不同表位并触发免疫反应 "的更正
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-19 DOI: 10.1111/mpp.13420

Niu Y, Fu S, Chen G, Wang H, Wang Y, Hu J, Jin X, Zhang M, Lu M, He Y, Wang D, Chen Y, Zhang Y, Coll N, Valls M, Zhao C, Chen Q and Lu H. Different epitopes of Ralstonia solanacearum effector RipAW are recognized by two Nicotiana species and trigger immune responses. Molecular Plant Pathology 2022;23:188–203

In the authorship section, the affiliations ‘Dongdong Wang2, Yong Zhang3,4, Núria S. Coll5, Marc Valls5,6, Qin Chen2 and Haibin Lu1,7’ (Author's affiliations) were incorrect. They should have read ‘Dongdong Wang3, Yong Zhang4,5, Núria S. Coll6, Marc Valls6,7, Qin Chen3 and Haibin Lu1,2

We apologize for these errors.

Niu Y, Fu S, Chen G, Wang H, Wang Y, Hu J, Jin X, Zhang M, Lu M, He Y, Wang D, Chen Y, Zhang Y, Coll N, Valls M, Zhao C, Chen Q and Lu H.两种烟草识别 Ralstonia solanacearum 效应体 RipAW 的不同表位并触发免疫反应。Molecular Plant Pathology 2022;23:188-203在作者姓名部分,"Dongdong Wang2, Yong Zhang3,4, Núria S. Coll5, Marc Valls5,6, Qin Chen2 and Haibin Lu1,7"(作者单位)有误,应为 "Dongdong Wang2, Yong Zhang3,4, Núria S. Coll5, Marc Valls5,6, Qin Chen2 and Haibin Lu1,7"。应为'Dongdong Wang3, Yong Zhang4,5, Núria S. Coll6, Marc Valls6,7, Qin Chen3 and Haibin Lu1,2'(作者单位有误,特此致歉)。
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引用次数: 0
Corrigendum to “Nicotiana benthamiana phosphatidylinositol 4-kinase type II regulates chilli leaf curl virus pathogenesis” 对 "烟草本芹磷脂酰肌醇 4- 激酶 II 型调控辣椒卷叶病毒致病机理 "的更正
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-19 DOI: 10.1111/mpp.13421

Mansi, Kushwaha, N.K., Singh, A.K., Karim, M.J. and Chakraborty, S. (2019) Nicotiana benthamiana phosphatidylinositol 4-kinase type II regulates chilli leaf curl virus pathogenesis. Molecular Plant Pathology, 20(10), 1408–1424. https://doi.org/10.1111/mpp.12846.

In the published version of this article in Figure 6, panels (d) and (e) were mistakenly used for both the NbPI4KII-mGFP + Rep1-180-DsRed and NbPI4KII-mGFP + Rep181-361-DsRed images. The two panels showing individual microscopy images with the NbPI4KII-mGFP + Rep1-180-DsRed and NbPI4KII-mGFP + Rep181-361-DsRed are highly identical; hence this mistake happened during figure assembly. This inadvertent figure error does not in any way alter the interpretations or the conclusions drawn in the manuscript. The corrected Figure 6 is shown below.

Details are in the caption following the image
FIGURE 6
Open in figure viewerPowerPoint
Colocalization study of NbPI4K-mGFP with Rep-DsRed and its mutant. Localization of NbPI4KII:mGFP with (a, b) Rep-DsRed, (c) Rep1-120-DsRed, (d) Rep1-180-DsRed and (e) Rep181-361-DsRed. Scale bar = 20 μm.

We apologize for this error.

Mansi, Kushwaha, N.K., Singh, A.K., Karim, M.J. and Chakraborty, S. (2019) Nicotiana benthamiana phosphatidylinositol 4-kinase type II regulates chilli leaf curl virus pathogenesis.Molecular Plant Pathology, 20(10), 1408-1424. https://doi.org/10.1111/mpp.12846.In 图 6 中这篇文章的出版版本中,(d)和(e)面板被错误地用于 NbPI4KII-mGFP + Rep1-180-DsRed 和 NbPI4KII-mGFP + Rep181-361-DsRed 图像。显示 NbPI4KII-mGFP + Rep1-180-DsRed 和 NbPI4KII-mGFP + Rep181-361-DsRed 的单个显微镜图像的两个面板是高度一致的;因此,这个错误是在拼图时发生的。这一疏忽造成的图表错误丝毫不会改变手稿中的解释或结论。更正后的图 6 如下所示。图 6在图查看器中打开PowerPoint NbPI4K-mGFP 与 Rep-DsRed 及其突变体的定位研究。NbPI4KII:mGFP 与 (a, b) Rep-DsRed、(c) Rep1-120-DsRed、(d) Rep1-180-DsRed 和 (e) Rep181-361-DsRed 的定位。缩放条 = 20 μm。
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引用次数: 0
WRR4B contributes to a broad-spectrum disease resistance against powdery mildew in Arabidopsis WRR4B 促进拟南芥对白粉病的广谱抗病性
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-08 DOI: 10.1111/mpp.13415
Shuangshuang Mei, Yuxin Song, Zuer Zhang, Haitao Cui, Shuguo Hou, Weiguo Miao, Wei Rong
Oidium heveae HN1106, a powdery mildew (PM) that infects rubber trees, has been found to trigger disease resistance in Arabidopsis thaliana through ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)-, PHYTOALEXIN DEFICIENT 4 (PAD4)- and salicylic acid (SA)-mediated signalling pathways. In this study, a typical TOLL-INTERLEUKIN 1 RECEPTOR, NUCLEOTIDE-BINDING, LEUCINE-RICH REPEAT (TIR-NB-LRR)-encoding gene, WHITE RUST RESISTANCE 4 (WRR4B), was identified to be required for the resistance against O. heveae in Arabidopsis. The expression of WRR4B was upregulated by O. heveae inoculation, and WRR4B positively regulated the expression of genes involved in SA biosynthesis, such as EDS1, PAD4, ICS1 (ISOCHORISMATE SYNTHASE 1), SARD1 (SYSTEMIC-ACQUIRED RESISTANCE DEFICIENT 1) and CBP60g (CALMODULIN-BINDING PROTEIN 60 G). Furthermore, WRR4B triggered self-amplification, suggesting that WRR4B mediated plant resistance through taking part in the SA-based positive feedback loop. In addition, WRR4B induced an EDS1-dependent hypersensitive response in Nicotiana benthamiana and contributed to disease resistance against three other PM species: Podosphaera xanthii, Erysiphe quercicola and Erysiphe neolycopersici, indicating that WRR4B is a broad-spectrum disease resistance gene against PMs.
研究发现,感染橡胶树的白粉病(PM)Oidium heveae HN1106 可通过增强抗病性 1(EDS1)、植物抗毒素缺乏 4(PAD4)和水杨酸(SA)介导的信号通路触发拟南芥的抗病性。在这项研究中,一个典型的 TOLL-INTERLEUKIN 1 RECEPTOR、NUCLEOTIDE-BINDING、LEUCINE-RICH REPEAT(TIR-NB-LRR)编码基因--白锈抗性 4(WRR4B)被确定为拟南芥抗性 O. heveae 的必需基因。WRR4B的表达受O. heveae接种的上调,并且WRR4B正向调节参与SA生物合成的基因的表达,如EDS1、PAD4、ICS1(ISOCHORISMATE SYNTHASE 1)、SARD1(SYSTEMIC-ACCIRED RESISTANCE DEFICIENT 1)和CBP60g(CALMODULIN-BINDING PROTEIN 60 G)。此外,WRR4B 还引发了自我扩增,这表明 WRR4B 通过参与基于 SA 的正反馈环路来介导植物抗性。此外,WRR4B 还诱导了烟草中依赖 EDS1 的超敏反应,并促进了对其他三种 PM 的抗病性:Podosphaera xanthii、Erysiphe quercicola 和 Erysiphe neolycopersici。
{"title":"WRR4B contributes to a broad-spectrum disease resistance against powdery mildew in Arabidopsis","authors":"Shuangshuang Mei, Yuxin Song, Zuer Zhang, Haitao Cui, Shuguo Hou, Weiguo Miao, Wei Rong","doi":"10.1111/mpp.13415","DOIUrl":"https://doi.org/10.1111/mpp.13415","url":null,"abstract":"<i>Oidium heveae</i> HN1106, a powdery mildew (PM) that infects rubber trees, has been found to trigger disease resistance in <i>Arabidopsis thaliana</i> through ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)-, PHYTOALEXIN DEFICIENT 4 (PAD4)- and salicylic acid (SA)-mediated signalling pathways. In this study, a typical <i>TOLL-INTERLEUKIN 1 RECEPTOR, NUCLEOTIDE-BINDING, LEUCINE-RICH REPEAT</i> (<i>TIR-NB-LRR</i>)-encoding gene, <i>WHITE RUST RESISTANCE 4</i> (<i>WRR4B</i>), was identified to be required for the resistance against <i>O. heveae</i> in <i>Arabidopsis</i>. The expression of <i>WRR4B</i> was upregulated by <i>O. heveae</i> inoculation, and <i>WRR4B</i> positively regulated the expression of genes involved in SA biosynthesis, such as <i>EDS1</i>, <i>PAD4</i>, <i>ICS1</i> (<i>ISOCHORISMATE SYNTHASE 1</i>), <i>SARD1</i> (<i>SYSTEMIC-ACQUIRED RESISTANCE DEFICIENT 1</i>) and <i>CBP60g</i> (<i>CALMODULIN-BINDING PROTEIN 60 G</i>). Furthermore, WRR4B triggered self-amplification, suggesting that WRR4B mediated plant resistance through taking part in the SA-based positive feedback loop. In addition, WRR4B induced an <i>EDS1</i>-dependent hypersensitive response in <i>Nicotiana benthamiana</i> and contributed to disease resistance against three other PM species: <i>Podosphaera xanthii</i>, <i>Erysiphe quercicola</i> and <i>Erysiphe neolycopersici</i>, indicating that <i>WRR4B</i> is a broad-spectrum disease resistance gene against PMs.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"86 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139410955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Infection-specific transcriptional patterns of the maize pathogen Cochliobolus heterostrophus unravel genes involved in asexual development and virulence 玉米病原体 Cochliobolus heterostrophus 的感染特异性转录模式揭示了涉及无性发育和毒力的基因
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-08 DOI: 10.1111/mpp.13413
Huilin Yu, Jiyue Zhang, Jinyu Fan, Wantong Jia, Yanan Lv, Hongyu Pan, Xianghui Zhang
Southern corn leaf blight (SCLB) caused by Cochliobolus heterostrophus is a destructive disease that threatens global maize (Zea mays) production. Despite many studies being conducted, very little is known about molecular processes employed by the pathogen during infection. There is a need to understand the fungal arms strategy and identify novel functional genes as targets for fungicide development. Transcriptome analysis based on RNA sequencing was carried out across conidia germination and host infection by C. heterostrophus. The present study revealed major changes in C. heterostrophus gene expression during host infection. Several differentially expressed genes (DEGs) induced during C. heterostrophus infection could be involved in the biosynthesis of secondary metabolites, peroxisome, energy metabolism, amino acid degradation and oxidative phosphorylation. In addition, histone acetyltransferase, secreted proteins, peroxisomal proteins, NADPH oxidase and transcription factors were selected for further functional validation. Here, we demonstrated that histone acetyltransferases (Hat2 and Rtt109), secreted proteins (Cel61A and Mep1), peroxisomal proteins (Pex11A and Pex14), NADPH oxidases (NoxA, NoxD and NoxR) and transcription factors (Crz1 and MtfA) play essential roles in C. heterostrophus conidiation, stress adaption and virulence. Taken together, our study revealed major changes in gene expression associated with C. heterostrophus infection and identified a diverse repertoire of genes critical for successful infection.
由异养杆孢菌(Cochliobolus heterostrophus)引起的南方玉米叶枯病(SCLB)是一种破坏性病害,威胁着全球玉米(Zea mays)的生产。尽管已经开展了许多研究,但人们对病原体在感染过程中所采用的分子过程知之甚少。有必要了解真菌的武器策略,并确定新的功能基因作为开发杀真菌剂的目标。基于 RNA 测序的转录组分析是在分生孢子萌发和宿主感染异养杆 菌期间进行的。本研究揭示了宿主感染期间异养真菌基因表达的主要变化。异养真菌感染期间诱导的几个差异表达基因(DEGs)可能涉及次级代谢产物的生物合成、过氧化物酶体、能量代谢、氨基酸降解和氧化磷酸化。此外,组蛋白乙酰转移酶、分泌蛋白、过氧化物酶体蛋白、NADPH 氧化酶和转录因子也被选作进一步的功能验证。在这里,我们证明了组蛋白乙酰转移酶(Hat2和Rtt109)、分泌蛋白(Cel61A和Mep1)、过氧物酶体蛋白(Pex11A和Pex14)、NADPH氧化酶(NoxA、NoxD和NoxR)和转录因子(Crz1和MtfA)在异养殖真菌的分生、应激适应和毒力中发挥着重要作用。总之,我们的研究揭示了与异养杆线虫感染相关的基因表达的主要变化,并确定了对成功感染至关重要的多种基因。
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引用次数: 0
Phytophthora infestans RXLR effector Pi23014 targets host RNA-binding protein NbRBP3a to suppress plant immunity Phytophthora infestans RXLR效应子Pi23014以宿主RNA结合蛋白NbRBP3a为靶标抑制植物免疫力
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-08 DOI: 10.1111/mpp.13416
Wanyue Li, Zeming Liu, Yuli Huang, Jie Zheng, Yang Yang, Yimeng Cao, Liwen Ding, Yuling Meng, Weixing Shan
Phytophthora infestans is a destructive oomycete that causes the late blight of potato and tomato worldwide. It secretes numerous small proteins called effectors in order to manipulate host cell components and suppress plant immunity. Identifying the targets of these effectors is crucial for understanding P. infestans pathogenesis and host plant immunity. In this study, we show that the virulence RXLR effector Pi23014 of P. infestans targets the host nucleus and chloroplasts. By using a liquid chromatogrpahy-tandem mass spectrometry assay and co-immunoprecipitation assasys, we show that it interacts with NbRBP3a, a putative glycine-rich RNA-binding protein. We confirmed the co-localization of Pi23014 and NbRBP3a within the nucleus, by using bimolecular fluorescence complementation. Reverse transcription-quantitative PCR assays showed that the expression of NbRBP3a was induced in Nicotiana benthamiana during P. infestans infection and the expression of marker genes for multiple defence pathways were significantly down-regulated in NbRBP3-silenced plants compared with GFP-silenced plants. Agrobacterium tumefaciens-mediated transient overexpression of NbRBP3a significantly enhanced plant resistance to P. infestans. Mutations in the N-terminus RNA recognition motif (RRM) of NbRBP3a abolished its interaction with Pi23014 and eliminated its capability to enhance plant resistance to leaf colonization by P. infestans. We further showed that silencing NbRBP3 reduced photosystem II activity, reduced host photosynthetic efficiency, attenuated Pi23014-mediated suppression of cell death triggered by P. infestans pathogen-associated molecular pattern elicitor INF1, and suppressed plant immunity.
Phytophthora infestans 是一种毁灭性的卵菌,在全球范围内导致马铃薯和番茄的晚疫病。它分泌大量被称为效应子的小蛋白,以操纵宿主细胞成分并抑制植物免疫。确定这些效应子的靶标对于了解 P. infestans 的致病机理和宿主植物免疫至关重要。在这项研究中,我们发现 P. infestans 的毒力 RXLR 效应子 Pi23014 以宿主细胞核和叶绿体为靶标。通过液相色谱-串联质谱分析和共免疫沉淀分析,我们发现它与NbRBP3a(一种假定的富含甘氨酸的RNA结合蛋白)相互作用。通过双分子荧光互补,我们证实了 Pi23014 和 NbRBP3a 在细胞核内的共定位。逆转录-定量 PCR 分析表明,在 P. infestans 感染期间,NbRBP3a 在烟草中的表达被诱导,与 GFP 沉默的植株相比,NbRBP3 沉默的植株中多种防御途径的标记基因的表达显著下调。农杆菌介导的 NbRBP3a 瞬时过表达显著增强了植物对 P. infestans 的抗性。NbRBP3a的N端RNA识别基序(RRM)发生突变后,它与Pi23014的相互作用消失了,其增强植物对侵染病菌叶片定殖的抗性的能力也消失了。我们进一步发现,沉默 NbRBP3 会降低光系统 II 的活性,降低宿主的光合效率,减弱 Pi23014 介导的对 P. infestans 病原体相关分子模式诱导剂 INF1 引发的细胞死亡的抑制作用,并抑制植物的免疫力。
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引用次数: 0
Metabolic variations in root tissues and rhizosphere soils of weak host plants potently lead to distinct host status and chemotaxis regulation of Meloidogyne incognita in intercropping. 弱寄主植物根组织和根际土壤的代谢变化可能导致间作中南方根结线虫不同的寄主地位和趋化性调节。
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-01 Epub Date: 2023-10-12 DOI: 10.1111/mpp.13396
Xu Zhang, Mengyuan Song, Lihong Gao, Yongqiang Tian

Root-knot nematodes (RKNs) inflict extensive damage to global agricultural production. Intercropping has been identified as a viable agricultural tool for combating RKNs, but the mechanisms by which intercropped plants modulate RKN parasitism are still not well understood. Here, we focus on the cucumber-amaranth intercropping system. We used a range of approaches, including the attraction assay, in vitro RNA interference (RNAi), untargeted metabolomics, and hairy root transformation, to unveil the mechanisms by which weak host plants regulate Meloidogyne incognita chemotaxis towards host plants and control infection. Amaranth roots showed a direct repellence to M. incognita through disrupting its chemotaxis. The in vitro RNAi assay demonstrated that the Mi-flp-1 and Mi-flp-18 genes (encoding FMRFamide-like peptides) regulated M. incognita chemotaxis towards cucumber and controlled infection. Moreover, M. incognita infection stimulated cucumber and amaranth to accumulate distinct metabolites in both root tissues and rhizosphere soils. In particular, naringenin and salicin, enriched specifically in amaranth rhizosphere soils, inhibited the expression of Mi-flp-1 and Mi-flp-18. In addition, overexpression of genes involved in the biosynthesis of pantothenic acid and phloretin, both of which were enriched specifically in amaranth root tissues, delayed M. incognita development in cucumber hairy roots. Together, our results reveal that both the distinct host status and disruption of chemotaxis contribute to M. incognita inhibition in intercropping.

根结线虫对全球农业生产造成广泛破坏。间作已被确定为对抗RKN的一种可行的农业工具,但间作植物调节RKN寄生的机制仍不清楚。在这里,我们重点介绍了黄瓜-苋间作系统。我们使用了一系列方法,包括吸引试验、体外RNA干扰(RNAi)、非靶向代谢组学和毛根转化,来揭示弱寄主植物调节南方根结线虫对寄主植物的趋化性和控制感染的机制。Amaranth根通过破坏其趋化性而对M.incognita表现出直接的排斥作用。体外RNAi测定表明,Mi-flp-1和Mi-flp-18基因(编码FMRF酰胺样肽)调节隐翅虫对黄瓜的趋化性并控制感染。此外,M.incognita感染刺激黄瓜和苋在根组织和根际土壤中积累不同的代谢产物。特别是在苋根际土壤中特异性富集的柚皮素和水杨素抑制了Mi-flp-1和Mi-flp-18的表达。此外,参与泛酸和根皮素生物合成的基因的过表达,这两种基因都在苋根组织中特异性富集,延缓了黄瓜毛状根中隐翅虫的发育。总之,我们的研究结果表明,不同的宿主状态和趋化性的破坏都有助于间作中M.incognita的抑制。
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引用次数: 0
The nanovirus U2 protein suppresses RNA silencing via three conserved cysteine residues. 纳米病毒U2蛋白通过三个保守的半胱氨酸残基抑制RNA沉默。
IF 4.9 1区 农林科学 Q1 PLANT SCIENCES Pub Date : 2024-01-01 Epub Date: 2023-10-12 DOI: 10.1111/mpp.13394
Dankan Yan, Kelei Han, Yuwen Lu, Jiejun Peng, Shaofei Rao, Guanwei Wu, Yong Liu, Jianping Chen, Hongying Zheng, Fei Yan

Nanoviruses have multipartite, circular, single-stranded DNA genomes and cause huge production losses in legumes and other crops. No viral suppressor of RNA silencing (VSR) has yet been reported from a member of the genus Nanovirus. Here, we demonstrate that the nanovirus U2 protein is a VSR. The U2 protein of milk vetch dwarf virus (MDV) suppressed the silencing of the green fluorescent protein (GFP) gene induced by single-stranded and double-stranded RNA, and the systemic spread of the GFP silencing signal. An electrophoretic mobility shift assay showed that the U2 protein was able to bind double-stranded 21-nucleotide small interfering RNA (siRNA). The cysteine residues at positions 43, 79 and 82 in the MDV U2 protein are critical to its nuclear localization, self-interaction and siRNA-binding ability, and were essential for its VSR activity. In addition, expression of the U2 protein via a potato virus X vector induced more severe necrosis symptoms in Nicotiana benthamiana leaves. The U2 proteins of other nanoviruses also acted as VSRs, and the three conserved cysteine residues were indispensable for their VSR activity.

纳米病毒具有多部分、环状、单链DNA基因组,并在豆类和其他作物中造成巨大的生产损失。尚未报道纳米病毒属成员的RNA沉默病毒抑制因子(VSR)。在这里,我们证明了纳米病毒U2蛋白是一种VSR。矮病毒(MDV)的U2蛋白抑制了单链和双链RNA诱导的绿色荧光蛋白(GFP)基因的沉默,以及GFP沉默信号的系统传播。电泳迁移率测定显示U2蛋白能够结合双链21核苷酸小干扰RNA(siRNA)。MDV U2蛋白中43、79和82位的半胱氨酸残基对其核定位、自相互作用和siRNA结合能力至关重要,并且对其VSR活性至关重要。此外,通过马铃薯病毒X载体表达U2蛋白在本氏烟草叶片中诱导了更严重的坏死症状。其他纳米病毒的U2蛋白也起到VSR的作用,三个保守的半胱氨酸残基对其VSR活性是必不可少的。
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Molecular plant pathology
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