Molecular plant pathology最新文献_第2页

Decursin, Identified via High-Throughput Chemical Screening, Enhances Plant Disease Resistance via Two Independent Mechanisms. 通过高通量化学筛选鉴定的Decursin通过两种独立的机制增强植物抗病性。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-06-01 DOI: 10.1111/mpp.70101

Yahui Ma, Yujie Zhao, Hanqi Huang, Yue Zhao, Rui Cao, Kunrong He, Lijuan Zhou, Yajin Ye

{"title":"Decursin, Identified via High-Throughput Chemical Screening, Enhances Plant Disease Resistance via Two Independent Mechanisms.","authors":"Yahui Ma, Yujie Zhao, Hanqi Huang, Yue Zhao, Rui Cao, Kunrong He, Lijuan Zhou, Yajin Ye","doi":"10.1111/mpp.70101","DOIUrl":"10.1111/mpp.70101","url":null,"abstract":"In order to overcome the damage caused by phytopathogens, plants have evolved a complex defence system to protect themselves, such as the two-tiered innate immunity system. Chemical screening has led to the identification of plant immune-priming compounds, which facilitate the functional dissection of the plant immune system and contribute to chemical control for plant diseases. In this study, we identified decursin, a coumarin natural product, through high-throughput screening for activators of the expression of FLG22-INDUCED RECEPTOR KINASE 1 (FRK1). Decursin functions as a typical immune elicitor, triggering early immune responses, including a reactive oxygen species (ROS) burst, MAPK activation, and transcriptional reprogramming of defence genes. A targeted reverse genetic approach identified CERK1, a lysin motif receptor-like kinase (LysM-RLK), loss of function of which resulted in a significant reduction of decursin-induced immune responses. Moreover, decursin was demonstrated to be ineffective in eliciting immune activation in the lyk4 lyk5 mutant, a double mutant of two additional LysM-RLKs. Molecular docking studies predicted that decursin may bind to CERK1 and LYK5. Decursin has been demonstrated to possess potent antiphytopathogenic properties, exhibiting pronounced growth inhibitory effects against several important plant fungal pathogens in vitro and in vivo, thereby protecting plants from damage caused by these pathogens. It can be concluded that decursin exerts its function through two independent mechanisms to enhance plant disease resistance, providing a potent agrochemical in disease control.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 6","pages":"e70101"},"PeriodicalIF":4.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12127108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diverse Genetic Mechanisms Enable Pseudomonas syringae to Rapidly Overcome Effector-Triggered Immunity. 不同的遗传机制使丁香假单胞菌能够快速克服效应触发免疫。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-06-01 DOI: 10.1111/mpp.70102

Jacy Newfeld, Elise Bull, Erka Shata, Mateja Perc, Rui Xuan Tang, Marcus M Dillon

{"title":"Diverse Genetic Mechanisms Enable Pseudomonas syringae to Rapidly Overcome Effector-Triggered Immunity.","authors":"Jacy Newfeld, Elise Bull, Erka Shata, Mateja Perc, Rui Xuan Tang, Marcus M Dillon","doi":"10.1111/mpp.70102","DOIUrl":"10.1111/mpp.70102","url":null,"abstract":"Bacterial plant pathogens pose a serious threat to worldwide crop yields and cause widespread food insecurity. One common approach to limit pathogen proliferation on critical crops is to genetically engineer cultivars that harbour resistance genes capable of recognising and responding to critical bacterial virulence factors like type III secreted effectors. Unfortunately, these resistance barriers are often overcome by pathogen evolution within just a few seasons. In this study, we explore the evolutionary mechanisms that enable pathogens to overcome plant resistance by leveraging two Pseudomonas syringae pv. maculicola strains that differ in their ability to cause disease on the model host Arabidopsis thaliana. We first characterise the molecular basis of the adaptation that enabled the P. syringae pv. maculicola PmaES4326 to overcome rps5-mediated resistance through a direct modification to its hopAR1 effector. We then show that through in planta evolution, the initially nonpathogenic strain P. syringae pv. maculicola PmaYM7930 can rapidly adapt to overcome rps5-mediated resistance via low-frequency mutations that do not involve direct modifications to hopAR1. This result was especially surprising because hopAR1 is known to be associated with mobile genetic elements that enable increased evolutionary plasticity. The rapid ability of P. syringae to overcome effector-triggered immunity without direct modifications to hopAR1 reveals that the genetic mechanisms enabling pathogens to overcome host resistance are more diverse than is currently recognised. This result has important implications for the development of more stably resistant crops that can resist various forms of pathogen evolution.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 6","pages":"e70102"},"PeriodicalIF":4.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12167760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Toxin of Valsa mali Determines Virulence and Host Preference. 马利缬草毒素决定毒力和寄主偏好。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-06-01 DOI: 10.1111/mpp.70106

Lin Tang, Liangliang Zhu, Xinyun Wu, Runze Tian, Yayuan Bai, Xiangrong Tian, Daoyuan Zhang, Lili Huang

{"title":"A Toxin of Valsa mali Determines Virulence and Host Preference.","authors":"Lin Tang, Liangliang Zhu, Xinyun Wu, Runze Tian, Yayuan Bai, Xiangrong Tian, Daoyuan Zhang, Lili Huang","doi":"10.1111/mpp.70106","DOIUrl":"10.1111/mpp.70106","url":null,"abstract":"Through co-evolutionary adaptation, phytopathogenic fungi have evolved specialised host preference mechanisms to optimise infection efficacy. Fungi of the Valsa genus infect various Rosaceae fruit trees, with Valsa mali exhibiting a marked host preference for apple trees, while Valsa pyri preferentially colonises pear trees. The divergent secondary metabolite biosynthetic gene clusters (SMBGCs) between these two species may serve as key determinants of their distinct host preferences. In this study, VmPKS5, a polyketide synthase, was identified as a key factor influencing the host preference of V. mali, which is the main pathogen of apple Valsa canker (AVC). Deletion of VmPKS5 greatly reduced the virulence of V. mali in apple trees, but not in pear trees. Deletion of VmPKS5 completely abolished the production of the toxin p-coumaric acid ethyl ester (p-CAEE). Exogenous p-CAEE application partly restored the virulence of ΔVmPKS5 and enhanced the virulence of the wild-type strain of V. mali. Crucially, heterologous expression of VmPKS5 in V. pyri increased its virulence towards apple trees by production of p-CAEE during infection. Notably, V. mali can uptake double-stranded RNA (dsRNA), and exogenous spray of VmPKS5-dsRNA significantly inhibited the infection by V. mali. This study provides new perspectives on host preference mechanisms of fungal pathogens and green disease control of tree disease by dsRNA fungicides.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 6","pages":"e70106"},"PeriodicalIF":4.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mutations in the SWEET15 Sugar Transporter Gene Affect Response of Citrus to Huanglongbing Disease and Citrus Canker. SWEET15糖转运基因突变影响柑橘对黄龙冰病和溃疡病的反应

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70094

Archana Khadgi, Omar Zayed, Cintia H D Sagawa, Fei Zhang, Danelle K Seymour, Vivian F Irish

{"title":"Mutations in the SWEET15 Sugar Transporter Gene Affect Response of Citrus to Huanglongbing Disease and Citrus Canker.","authors":"Archana Khadgi, Omar Zayed, Cintia H D Sagawa, Fei Zhang, Danelle K Seymour, Vivian F Irish","doi":"10.1111/mpp.70094","DOIUrl":"10.1111/mpp.70094","url":null,"abstract":"Bacterial diseases like huanglongbing (HLB) and citrus canker severely impact citrus production. HLB, caused by \"Candidatus Liberibacter asiaticus\" (CLas), leads to tree decline, while citrus canker, caused by Xanthomonas citri pv. citri (Xcc) causes necrotic lesions on leaves and fruit. Many bacterial pathogens secrete effector proteins that suppress host plant immunity and promote pathogenesis through the upregulation of host-encoded susceptibility genes. Xcc uses the type III secretion system to introduce effector proteins such as the transcription factor-like (TAL) effector PthA4 that can directly activate host susceptibility gene expression. In contrast, CLas lacks most bacterial secretion systems and relies predominantly on the Sec secretion system for pathogenesis. While some Sec-secreted proteins have been identified in CLas, their direct role in causing HLB symptoms remains unproven. Several Sugars Will Eventually be Exported Transporter (SWEET) genes, encoding sucrose transporters, are candidate susceptibility genes. Here we investigate the roles of the citrus SWEET10, SWEET12 and SWEET15 genes and show that mutations of SWEET15 resulted in reduced susceptibility to citrus canker in three different citrus cultivars: Carrizo citrange (Citrus sinensis 'Washington' sweet orange × Poncirus trifoliata), 'Limoneria 8A' Lisbon lemon (Citrus limon) and 'Pineapple' sweet orange (C. sinensis). Furthermore, Lisbon lemon plants mutated for SWEET15 also showed reduced CLas titre in infected plants. These results suggest that SWEET15 may act as a broad-spectrum susceptibility gene, and disruption of SWEET15 gene activity could be a viable approach to mitigating bacterial diseases such as citrus canker and HLB in a variety of citrus cultivars.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70094"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Betulinic Acid Delays Turnip Mosaic Virus Infection by Activating the Phytosulfokine Signalling Pathway in Nicotiana benthamiana. 白桦酸通过激活植物硫代素信号通路延缓萝卜花叶病毒感染。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70092

Meirong Xiang, Pengyue Wang, Keda Han, Jianjian Liu, Ziting Huang, Chaonan Wang, Xinxin Jing, Jiao Du, Bingjian Sun, Honglian Li, Chao Zhang, Pengbai Li

{"title":"Betulinic Acid Delays Turnip Mosaic Virus Infection by Activating the Phytosulfokine Signalling Pathway in Nicotiana benthamiana.","authors":"Meirong Xiang, Pengyue Wang, Keda Han, Jianjian Liu, Ziting Huang, Chaonan Wang, Xinxin Jing, Jiao Du, Bingjian Sun, Honglian Li, Chao Zhang, Pengbai Li","doi":"10.1111/mpp.70092","DOIUrl":"https://doi.org/10.1111/mpp.70092","url":null,"abstract":"Plant viral diseases pose a significant threat to agricultural production, and the availability of effective drugs against viral diseases remains limited. In this study, we discovered that betulinic acid (BA), a pentacyclic triterpenoid derived from plants, delays infection by turnip mosaic virus (TuMV) in Nicotiana benthamiana. Transcriptomic analysis revealed that BA treatment specifically induced the expression of N. benthamiana phytosulfokine 3 (NbPSK3), a plant pentapeptide hormone with diverse functions, while TuMV infection suppressed its expression. Further study demonstrated that NbPSK3 positively regulates antiviral defence against TuMV infection. Disruption of PSK signalling by targeting the membrane-bound PSK receptors (PSKRs) promoted viral infection. Additionally, exogenous sulphonated PSK (active form) treatment significantly delayed infection by TuMV in N. benthamiana compared to unmodified PSK peptides (dPSK, inactive form) or control treatments, while silencing the receptor NbPSKR1 abolished the ability of PSK to inhibit TuMV infection. Moreover, the inhibition of TuMV infection by BA is dependent on the PSK-PSKR signalling pathway. Overall, these findings not only underscore the potential of BA as a promising and environmentally friendly agent for modulating plant viral diseases but also emphasise the role of the PSK signalling pathway in promoting at least partial resistance to TuMV, which might have interest for crop breeding.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70092"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12066822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting of the Hybrid Bamboo BDDnaJ by Pathogen Effector ApcE12 Regulates the Unfolded Protein Response. 病原效应物ApcE12靶向杂交竹BDDnaJ调控未折叠蛋白反应

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70089

Fengying Luo, Xinmei Fang, Haiyan Luo, Ziqi Ye, Sijia Liu, Han Zhao, Shuying Li, Shujiang Li

{"title":"Targeting of the Hybrid Bamboo BDDnaJ by Pathogen Effector ApcE12 Regulates the Unfolded Protein Response.","authors":"Fengying Luo, Xinmei Fang, Haiyan Luo, Ziqi Ye, Sijia Liu, Han Zhao, Shuying Li, Shujiang Li","doi":"10.1111/mpp.70089","DOIUrl":"https://doi.org/10.1111/mpp.70089","url":null,"abstract":"The shoot blight disease of Bambusa pervariabilis × Dendrocalamopsis grandis, caused by Arthrinium phaeospermum, threatens bamboo's ecological and economic value. This study explores the pathogenic effector ApcE12's role in modulating plant immunity through interactions with the host proteins BDClp and BDDnaJ. ApcE12 directly interacts with BDDnaJ, a vital regulator of the unfolded protein response (UPR), as validated through yeast two-hybrid, bimolecular fluorescence complementation, and GST pull-down assays. Functional analyses demonstrated that silencing BDDnaJ reduces UPR, activating programmed cell death (PCD) and blocking further pathogen infection to enhance plant resistance. BDDnaJ was found to regulate BDBiP protein stability by interacting with BDBiP, and it is this mechanism by which the pathogenic effector ApcE12 regulates BDDnaJ expression, enhances UPR signalling, and inhibits PCD, thereby promoting infection. These findings deepen our understanding of how fungal effectors manipulate UPR and PCD to overcome plant defences, providing novel insights for developing resistance strategies in bamboo species.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70089"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12040440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasmopara viticola Effector PvRXLR10 Targets a Host Phospholipase VvipPLA-IIδ2 to Suppress Plant Immunity in Grapevine. 葡萄原浆原效应物PvRXLR10靶向宿主磷脂酶VvipPLA-IIδ2抑制葡萄植物免疫

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70095

Junjie Qu, Lulu Liu, Chengxu Zheng, Zexi Guo, Dayun Sun, Fengying Pan, Jiang Lu, Ling Yin

{"title":"Plasmopara viticola Effector PvRXLR10 Targets a Host Phospholipase VvipPLA-IIδ2 to Suppress Plant Immunity in Grapevine.","authors":"Junjie Qu, Lulu Liu, Chengxu Zheng, Zexi Guo, Dayun Sun, Fengying Pan, Jiang Lu, Ling Yin","doi":"10.1111/mpp.70095","DOIUrl":"10.1111/mpp.70095","url":null,"abstract":"Plasmopara viticola that causes grapevine downy mildew disease in viticulture regions is among the 10 most relevant pathogens worldwide. It secretes a large arsenal of effectors to facilitate colonisation by perturbing host immunity. However, the underlying mechanisms by which P. viticola effectors disturb grapevine defence are still largely unknown. In this study, we report that PvRXLR10, an RXLR effector with a WY domain, promotes P. viticola infection in grapevine and Phytophthora parasitica colonisation in Nicotiana benthamiana. PvRXLR10 interacts with a host patatin-like protein VvipPLA-IIδ2 with phospholipase A2 activity. The WY domain of PvRXLR10 is not responsible for cell death suppression in N. benthamiana but is necessary for PvRXLR10 interaction with VvipPLA-IIδ2. Overexpression and RNAi-mediated suppression of VvipPLA-IIδ2 expression in Vitis vinifera consistently showed that this protein positively regulates plant immunity in response to P. viticola infection. Interestingly, we found that VvipPLA-IIδ2 partially associates with PvRXLR10 at the endoplasmic reticulum (ER). Reverse transcription-quantitative PCR (RT-qPCR) analysis showed that the expression of VvipPLA-IIδ2 was suppressed by PvRXLR10 during P. viticola infection. The overexpression of VvipPLA-IIδ2 in V. vinifera induced higher expression of genes related to jasmonic acid (JA) biosynthesis, signalling pathways and defence response. The evidence indicates the important roles of VvipPLA-IIδ2 in grapevine immunity and P. viticola effector PvRXLR10 targets this protein to promote its infection.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70095"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Valsa mali Effector VmSR1 Accelerates the Degradation of Tudor-SN2 to Suppress RNA Silencing and Plant Immunity. Valsa mali效应物VmSR1加速Tudor-SN2降解抑制RNA沉默和植物免疫

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70097

Tao Jiang, Chengli Wang, Mian Zhang, Yongli Qiao, Zhensheng Kang, Lili Huang

引用次数: 0

Pseudomonas syringae pv. tabaci 6605 Requires Seven Type III Effectors to Infect Nicotiana benthamiana. 丁香假单胞菌。烟草6605需要7种III型效应器来感染本烟菌。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70091

Kana Kuroe, Takafumi Nishimura, Sachi Kashihara, Nanami Sakata, Mikihiro Yamamoto, Yoshiteru Noutoshi, Kazuhiro Toyoda, Yuki Ichinose, Hidenori Matsui

{"title":"Pseudomonas syringae pv. tabaci 6605 Requires Seven Type III Effectors to Infect Nicotiana benthamiana.","authors":"Kana Kuroe, Takafumi Nishimura, Sachi Kashihara, Nanami Sakata, Mikihiro Yamamoto, Yoshiteru Noutoshi, Kazuhiro Toyoda, Yuki Ichinose, Hidenori Matsui","doi":"10.1111/mpp.70091","DOIUrl":"https://doi.org/10.1111/mpp.70091","url":null,"abstract":"Type III effectors (T3Es), virulence factors injected into plant cells via the type III secretion system (T3SS), play essential roles in the infection of host plants. Pseudomonas syringae pv. tabaci 6605 (Pta 6605) is the causal agent of wildfire disease in tobacco and harbours at least 22 T3Es in its genome. However, the specific T3Es required by Pta 6605 to infect Nicotiana benthamiana remain unidentified. In this study, we investigated the T3Es that contribute to Pta 6605 infection of N. benthamiana. We constructed Pta 6605 poly-T3E-deficient mutants (Pta DxE) and inoculated them into N. benthamiana. Flood assay, which mimics natural opening-based entry, showed that mutant strains lacking 14-22 T3Es, namely, Pta D14E-D22E mutants, exhibited reduced disease symptoms. By contrast, infiltration inoculation, which involves direct injection into leaves, showed that the Pta D14E to Pta D20E mutants developed disease symptoms. Notably, the Pta D20E, containing AvrE1 and HopM1, induced weak but observable symptoms upon infiltration inoculation. Conversely, no symptoms were observed in either the flood assay or infiltration inoculation for Pta D21E and Pta D22E. Taken together, these findings indicate that the many T3Es such as AvrPto4/AvrPtoB, HopW1/HopAE1, and HopM1/AvrE1 in Pta 6605 collectively contribute to invasion through natural openings and symptom development in N. benthamiana. This study provides the basis for understanding virulence in the host by identifying the minimum T3E repertoire required by Pta 6605 to infect N. benthamiana.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70091"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144024966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genomic Islands of Pseudomonas syringae pv. tabaci 6605: Identification of PtaGI-1 as a Pathogenicity Island With Effector Genes and a Tabtoxin Cluster. 丁香假单胞菌基因组岛。烟草6605:PtaGI-1致病性岛与效应基因的鉴定和一个烟草毒素簇。

IF 4.8 1区农林科学

Molecular plant pathology Pub Date : 2025-05-01 DOI: 10.1111/mpp.70087

Yuta Watanabe, Kotomi Kunishi, Hidenori Matsui, Nanami Sakata, Yoshiteru Noutoshi, Kazuhiro Toyoda, Yuki Ichinose

{"title":"Genomic Islands of Pseudomonas syringae pv. tabaci 6605: Identification of PtaGI-1 as a Pathogenicity Island With Effector Genes and a Tabtoxin Cluster.","authors":"Yuta Watanabe, Kotomi Kunishi, Hidenori Matsui, Nanami Sakata, Yoshiteru Noutoshi, Kazuhiro Toyoda, Yuki Ichinose","doi":"10.1111/mpp.70087","DOIUrl":"10.1111/mpp.70087","url":null,"abstract":"Genomic islands (GIs) are 20-500 kb DNA regions that are thought to be acquired by horizontal gene transfer. GIs that confer pathogenicity and environmental adaptation have been reported in Pseudomonas species; however, GIs that enhance bacterial virulence have not. Here, we identified 110 kb and 103 kb GIs in P. syringae pv. tabaci 6605 (Pta6605), the causative agent of tobacco wildfire disease, which has the ability to produce tabtoxin as a phytotoxin. These GIs are partially homologous to known genomic islands in Pseudomonas aeruginosa and P. syringae pv. phaseolicola and were designated PtaGI-1 and PtaGI-2. Both PtaGIs conserve core genes, whereas each GI possesses different accessory genes. PtaGI-1 contains a tabtoxin biosynthetic gene cluster and three type III effector genes among its accessory genes, whereas PtaGI-2 also contains homologous genes to hsvABC, pathogenicity-related genes in Erwinia amylovora. Inoculation revealed that the PtaGI-1 mutant, but not the PtaGI-2 mutant, lost the ability to biosynthesise tabtoxin and to cause disease. Therefore, PtaGI-1 is thought to be a pathogenicity island. Both PtaGI-1 and PtaGI-2 have a pseudogene of tRNALys on the left border and an intact tRNALys gene on the right border. In a colony of Pta6605, both GIs can be excised at tRNALys, and PtaGI-1 and PtaGI-2 exist in a circular form. These results indicate that tabtoxin biosynthesis genes in PtaGI-1 are required for disease development, and PtaGI-1 is necessary for Pta6605 virulence.","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"26 5","pages":"e70087"},"PeriodicalIF":4.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0