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学者姓名：吴建国
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Abstract ：
本发明公开了miR1868在调控水稻分蘖和抗病毒中的应用，本方案提供了基因Osa‑miR1868(简称miR1868)和Pre‑miR1868(miR1868前体)在调控植物分蘖和对病毒病抗性中的应用；本方案将编码Pre‑miR1868的DNA分子导入目的的植物，得到转基因植物，所述转基因植物的分蘖少于受体植物，但是抗病性高于受体植物。说明Pre‑miR1868超量表达减少了植物分蘖，但是提高了植物对病毒病的耐受性。Pre‑miR1868具有调控植物分蘖和病毒抗性的功能，对于培育抗病毒植物，提高植物产量具有重大价值。
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| GB/T 7714 | 吴建国 , 张宝刚 , 张帅 et al. miR1868在调控水稻分蘖和抗病毒中的应用 : CN202411014313.2[P]. | 2024-07-26 . |
| MLA | 吴建国 et al. "miR1868在调控水稻分蘖和抗病毒中的应用" : CN202411014313.2. | 2024-07-26 . |
| APA | 吴建国 , 张宝刚 , 张帅 , 赵珊珊 , 张雄 . miR1868在调控水稻分蘖和抗病毒中的应用 : CN202411014313.2. | 2024-07-26 . |
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Leaf morphogenesis is essential for plant growth and development, yet the mechanisms by which plant viruses induce changes in leaf shape are not well understood. Rice ragged stunt virus (RRSV) infection induces distinct morphological abnormalities in rice leaves, including leaf tip curling and serrated margins, through unknown pathogenic mechanisms. This study reveals that key regulatory microRNAs (miR164, miR319 and miR156) and their target genes (CUC, TCP and SPL) exhibit entirely opposite expression patterns in healthy and RRSV-infected leaves, indicating a profound impact on the leaf morphogenesis network. Significantly, the core protein OsCUC1, which typically functions by forming dimers, shows abnormal expression in the peripheral zone of the shoot apical meristem under viral infection, leading to disruptions in leaf development. OsTCP1 was found to dynamically regulate OsCUC1 dimer formation by modifying its subcellular localization and interacting with OsSPL14 and OsSPL17, thereby influencing their regulatory functions. Genetic disruptions of OsCUC1, OsTCP1 and OsSPL14/OsSPL17 enhance the severity of RRSV infection, demonstrating their critical involvement in the viral pathogenic strategy. The research uncovers a novel mechanism by which RRSV manipulates the expression and interactions of key regulatory factors, disrupting the delicate balance of the leaf morphogenesis network. These findings expand our understanding of viral manipulation of host development and provide a foundation for innovative strategies to enhance crop resilience.
Keyword ：
leaf morphogenesis leaf morphogenesis miR156/164/319 miR156/164/319 OsCUC1/TCP1/SPL14 OsCUC1/TCP1/SPL14 RRSV RRSV
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| GB/T 7714 | Wang, Lu , Wu, Yuansheng , Zhang, Jialin et al. Spatial Regulation of Rice Leaf Morphology by miRNA-Target Complexes During Viral Infection [J]. | PLANT CELL AND ENVIRONMENT , 2025 , 48 (6) : 4625-4642 . |
| MLA | Wang, Lu et al. "Spatial Regulation of Rice Leaf Morphology by miRNA-Target Complexes During Viral Infection" . | PLANT CELL AND ENVIRONMENT 48 . 6 (2025) : 4625-4642 . |
| APA | Wang, Lu , Wu, Yuansheng , Zhang, Jialin , Li, Shanshan , Ren, Junjie , Yang, Liyuan et al. Spatial Regulation of Rice Leaf Morphology by miRNA-Target Complexes During Viral Infection . | PLANT CELL AND ENVIRONMENT , 2025 , 48 (6) , 4625-4642 . |
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While RNA silencing is crucial for plant resistance against viruses, the cellular connections between RNA silencing and antiviral responses in plants remain poorly understood. In this study, we aim to investigate this relationship by examining the subcellular localization of small RNA loading and viral replication in Arabidopsis. Our findings reveal that Argonaute 2 (AGO2), a key component of RNA silencing, loads small RNAs at the endoplasmic reticulum (ER)-chloroplast membrane contact sites (MCSs). We identify a chloroplast-localized protein, RNA helicase 3 (RH3), which interacts with AGO2 and facilitates the loading of small RNAs into AGO2 at these MCSs. Furthermore, we discover that MCSs serve as replication sites for certain plant viruses. RH3 also promotes the loading of viral-derived small RNAs into AGO2, thereby enhancing plant antiviral resistance. Overall, our study sheds light on the roles of RH3 in RNA silencing and plant antiviral defenses, providing valuable insights into the cytobiological connections between RNA silencing, viral replication, and antiviral immunity.
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| GB/T 7714 | Huang, Juan , Du, Juan , Liu, Yan et al. RH3 enhances antiviral defense by facilitating small RNA loading into Argonaute 2 at endoplasmic reticulum-chloroplast membrane contact sites [J]. | NATURE COMMUNICATIONS , 2025 , 16 (1) . |
| MLA | Huang, Juan et al. "RH3 enhances antiviral defense by facilitating small RNA loading into Argonaute 2 at endoplasmic reticulum-chloroplast membrane contact sites" . | NATURE COMMUNICATIONS 16 . 1 (2025) . |
| APA | Huang, Juan , Du, Juan , Liu, Yan , Lu, Lu , Xu, Yanzhuo , Shi, Jianfei et al. RH3 enhances antiviral defense by facilitating small RNA loading into Argonaute 2 at endoplasmic reticulum-chloroplast membrane contact sites . | NATURE COMMUNICATIONS , 2025 , 16 (1) . |
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The present disclosure locates a new brown planthopper resistance gene BPH33.2 on the short arm of rice chromosome 4 by extreme mixed pool analysis (BSA-seq), and genetically transforming the gene BPH33.2 to make the susceptible rice to be the brown planthopper resistant phenotype rice; at the same time, the knockout of the gene BPH33.2 was used to cause the loss of the brown planthopper resistant phenotype in insect resistant rice, thus confirming the function of BPH33.2. The present disclosure also provides molecular markers closely linked with the rice brown planthopper resistance gene BPH33.2. Through experimental detection of molecular markers linked or co-segregated with these resistance loci, the brown planthopper resistance of rice plants can be accurately predicted at the seedling stage, accelerating the progress of the selection of brown planthopper-resistant rice varieties.
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| GB/T 7714 | JIANGUO WU , JIE HU , SHUAI ZHANG et al. METHOD FOR PREPARING BROWN PLANTHOPPER RESISTANT PLANTS USING RICE BROWN PLANTHOPPER RESISTANCE GENE BPH33.2 : US202418414498A[P]. | 2024-01-17 . |
| MLA | JIANGUO WU et al. "METHOD FOR PREPARING BROWN PLANTHOPPER RESISTANT PLANTS USING RICE BROWN PLANTHOPPER RESISTANCE GENE BPH33.2" : US202418414498A. | 2024-01-17 . |
| APA | JIANGUO WU , JIE HU , SHUAI ZHANG , SHANSHAN ZHAO , XIAOQING WU . METHOD FOR PREPARING BROWN PLANTHOPPER RESISTANT PLANTS USING RICE BROWN PLANTHOPPER RESISTANCE GENE BPH33.2 : US202418414498A. | 2024-01-17 . |
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Plant diseases, caused by a wide range of pathogens, severely reduce crop yield and quality, posing a significant threat to global food security. Developing broad-spectrum resistance (BSR) in crops is a key strategy for controlling crop diseases and ensuring sustainable crop production. Cloning disease-resistance (R) genes and understanding their underlying molecular mechanisms provide new genetic resources and strategies for crop breeding. Novel genetic engineering and genome editing tools have accelerated the study and engineering of BSR genes in crops, which is the primary focus of this review. We first summarize recent advances in understanding the plant immune system, followed by an examination of the molecular mechanisms underlying BSR in crops. Finally, we highlight diverse strategies employed to achieve BSR, including gene stacking to combine multiple R genes, multiplexed genome editing of susceptibility genes and promoter regions of executor R genes, editing cis-regulatory elements to fine-tune gene expression, RNA interference, saturation mutagenesis, and precise genomic insertions. The genetic studies and engineering of BSR are accelerating the breeding of disease-resistant cultivars, contributing to crop improvement and enhancing global food security.
Keyword ：
broad-spectrum resistance broad-spectrum resistance genetic engineering genetic engineering genome editing genome editing knock-in knock-in Oryza sativa Oryza sativa Triticum aestivum Triticum aestivum
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| GB/T 7714 | Han, Xinyu , Li, Shumin , Zeng, Qingdong et al. Genetic engineering, including genome editing, for enhancing broad-spectrum disease resistance in crops [J]. | PLANT COMMUNICATIONS , 2025 , 6 (2) . |
| MLA | Han, Xinyu et al. "Genetic engineering, including genome editing, for enhancing broad-spectrum disease resistance in crops" . | PLANT COMMUNICATIONS 6 . 2 (2025) . |
| APA | Han, Xinyu , Li, Shumin , Zeng, Qingdong , Sun, Peng , Wu, Dousheng , Wu, Jianguo et al. Genetic engineering, including genome editing, for enhancing broad-spectrum disease resistance in crops . | PLANT COMMUNICATIONS , 2025 , 6 (2) . |
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Liquid-liquid phase separation (LLPS) regulates diverse biological functions by mediating the assembly of biomolecular condensates. However, it remains unclear how host LLPS is targeted by viruses during infection. Here we show that a plant bunyaviral protein, the disease-specific protein (SP) encoded by rice stripe virus (RSV), possesses phase separation potential through its N-terminal intrinsically disordered region 1 (IDR1). In vivo, however, SP does not form phase-separated biomolecular condensates independently but utilizes its phase separation properties to interfere with the phase separation of the SERRATE protein (SE), a key component of Dicing bodies essential for microRNA processing. By disrupting SE phase separation, SP inhibits D-body assembly and miRNA biogenesis. Our study demonstrates that a viral protein can modulate host microRNA processing by targeting LLPS, revealing a previously uncharacterized mechanism involved in viral infection strategies and miRNA biogenesis regulation in plants.
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| GB/T 7714 | Zou, Jing , Zhang, Shuai , Chen, Ying et al. A plant bunyaviral protein disrupts SERRATE phase separation to modulate microRNA biogenesis during viral pathogenesis [J]. | NATURE COMMUNICATIONS , 2025 , 16 (1) . |
| MLA | Zou, Jing et al. "A plant bunyaviral protein disrupts SERRATE phase separation to modulate microRNA biogenesis during viral pathogenesis" . | NATURE COMMUNICATIONS 16 . 1 (2025) . |
| APA | Zou, Jing , Zhang, Shuai , Chen, Ying , He, Chun , Pan, Xin , Zhang, Yimin et al. A plant bunyaviral protein disrupts SERRATE phase separation to modulate microRNA biogenesis during viral pathogenesis . | NATURE COMMUNICATIONS , 2025 , 16 (1) . |
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N REQUIREMENT GENE 1 (NRG1) is a pivotal player in the basal immune system and in Toll/Interleukin-1 receptor nucleotide-binding domain leucine-rich repeat (TNL)-mediated effector-triggered immunity (ETI), yet its transcriptional regulation remains poorly investigated. In this study, we identified NbWRKY7, a WRKY transcription factor that enhances both basal immunity and TNL-mediated ETI by regulating NRG1 transcription and accumulation. NbWRKY7 directly binds to the W-box cis-elements within the NRG1 promoter and induces its transcription. Silencing NbWRKY7 compromises basal defense and impairs TNL-mediated resistance to both viral and bacterial pathogens, as well as hypersensitive response-type programmed cell death (HR-PCD). Notably, effectors trigger resistosome formation to activate NRG1-dependent immune responses, which, in turn, further enhance NbWRKY7 transcription, thereby reinforcing NRG1 transcription. The WRKY7-NRG1 module orchestrates TNL-mediated immune responses through a positive feedback loop in Nicotiana benthamiana. Our findings provide a perspective on the regulatory mechanisms of NRG1 during basal and TNL-mediated immune responses, offering insights into the complex interplay of transcription factors in plant immunity. The transcription factor WRKY7-immunity protein NRG1 module forms a positive feedback loop that amplifies plant basal immunity and TNL receptor-mediated effector-triggered immunity.
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| GB/T 7714 | Wu, Ming , Zheng, Xiyin , Hu, Maohong et al. WRKY7 positively regulates plant immunity by transcriptionally activating N REQUIREMENT GENE 1 in Nicotiana benthamiana [J]. | PLANT PHYSIOLOGY , 2025 , 199 (2) . |
| MLA | Wu, Ming et al. "WRKY7 positively regulates plant immunity by transcriptionally activating N REQUIREMENT GENE 1 in Nicotiana benthamiana" . | PLANT PHYSIOLOGY 199 . 2 (2025) . |
| APA | Wu, Ming , Zheng, Xiyin , Hu, Maohong , Zhang, Danfeng , Lei, Xin , Han, Meng et al. WRKY7 positively regulates plant immunity by transcriptionally activating N REQUIREMENT GENE 1 in Nicotiana benthamiana . | PLANT PHYSIOLOGY , 2025 , 199 (2) . |
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Rice, a major global food staple, is threatened by viral infections that hinder its growth and yield. We have recently shown that the virulence protein P3 of rice grassy stunt virus promotes pathogenesis by inducing proteasome-controlled degradation of the rice RNA polymerase IV (RNA Pol IV) protein NRPD1a controlled by the P3-interacting E3 ubiquitin ligase P3IP1. However, the underlying mechanisms remain elusive. In this study, we show that P3 acts as a virus-encoded transcription activator-like effector to upregulate transcription of somatic embryogenesis receptor kinase 4 (SERK4) by directly binding to its promoter. SERK4 phosphorylates P3IP1 and enhances RNA Pol IVa (NRPD1a) degradation following P3IP1-controlled ubiquitination, leading to attenuated antiviral defense in rice. Thus, our study finds a critical viral virulence strategy by encoding a transcription factor-like protein that activates a host kinase to promote proteasome-controlled degradation of NRPD1a, thereby disarming RNA-directed DNA methylation (RdDM) antiviral defense.
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| GB/T 7714 | Wu, Yuansheng , Zhao, Shanshan , Liu, Na et al. A virulence protein activates SERK4 and degrades RNA polymerase IV protein to suppress rice antiviral immunity [J]. | DEVELOPMENTAL CELL , 2025 , 60 (17) : 2348-2362 . |
| MLA | Wu, Yuansheng et al. "A virulence protein activates SERK4 and degrades RNA polymerase IV protein to suppress rice antiviral immunity" . | DEVELOPMENTAL CELL 60 . 17 (2025) : 2348-2362 . |
| APA | Wu, Yuansheng , Zhao, Shanshan , Liu, Na , Wu, Fengling , Huang, Shiting , Li, Dongyuan et al. A virulence protein activates SERK4 and degrades RNA polymerase IV protein to suppress rice antiviral immunity . | DEVELOPMENTAL CELL , 2025 , 60 (17) , 2348-2362 . |
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Remarkable phenotypic plasticity of phytoplasma infections stems from the fast evolution and functional divergence of a versatile effector arsenal. We first catalogue more than 50 characterised effectors, highlighting their interference with SPL/GATA, TCP, MADS-box and ARF hubs, and the combined consequences for plant morphogenesis, hormone homoeostasis and vector colonisation. We then explain how drastic genome reduction coexists with extensive repeats and is balanced by PMU-mediated replication and recombination to maintain genetic flexibility. Comparisons at the population level indicate that most effectors are located on PMUs, which promote the evolution of effectors through recombination, replication and horizontal transfer. Purifying selection preserves essential virulence functions and eliminates mutations that compromise effector activity, while diversifying selection fine-tunes host specificity and may aid evasion of host immune responses. Finally, we argue that elucidating the mechanistic link between the dynamics of PMUs and effector evolution may provide deeper insights into the molecular mechanisms of host manipulation.
Keyword ：
effector proteins effector proteins horizontal gene transfer horizontal gene transfer host-pathogen interaction host-pathogen interaction phytoplasma phytoplasma potential mobile units potential mobile units
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| GB/T 7714 | Gan, Peng , Yu, Xiyuan , Zou, Jing et al. Evolution and Functional Adaptation of Phytoplasma Effectors: A Potential Mobile Unit-Driven Perspective [J]. | PLANT CELL AND ENVIRONMENT , 2025 . |
| MLA | Gan, Peng et al. "Evolution and Functional Adaptation of Phytoplasma Effectors: A Potential Mobile Unit-Driven Perspective" . | PLANT CELL AND ENVIRONMENT (2025) . |
| APA | Gan, Peng , Yu, Xiyuan , Zou, Jing , Li, Chuan , Yao, Zhitong , Ye, Yangdong et al. Evolution and Functional Adaptation of Phytoplasma Effectors: A Potential Mobile Unit-Driven Perspective . | PLANT CELL AND ENVIRONMENT , 2025 . |
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| GB/T 7714 | Wu, Ming , Zhao, Shanshan , Wu, Jianguo . Simple but effective: Minimalist NLR rewiring, maximal virus resistance [J]. | MOLECULAR PLANT , 2025 , 18 (11) : 1803-1805 . |
| MLA | Wu, Ming et al. "Simple but effective: Minimalist NLR rewiring, maximal virus resistance" . | MOLECULAR PLANT 18 . 11 (2025) : 1803-1805 . |
| APA | Wu, Ming , Zhao, Shanshan , Wu, Jianguo . Simple but effective: Minimalist NLR rewiring, maximal virus resistance . | MOLECULAR PLANT , 2025 , 18 (11) , 1803-1805 . |
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