Bryce G Alex, Zong-Ying Zhang, Danny Lasky, Hernan Garcia-Ruiz, Ronnie Dewberry, Caitilyn Allen, Dennis Halterman, Aurélie M Rakotondrafara
{"title":"A single phosphorylatable amino acid residue is essential for the recognition of multiple potyviral HCPro effectors by potato Ny<sub>tbr</sub>.","authors":"Bryce G Alex, Zong-Ying Zhang, Danny Lasky, Hernan Garcia-Ruiz, Ronnie Dewberry, Caitilyn Allen, Dennis Halterman, Aurélie M Rakotondrafara","doi":"10.1111/mpp.70027","DOIUrl":"10.1111/mpp.70027","url":null,"abstract":"<p><p>Potato virus Y (PVY, Potyviridae) is among the most important viral pathogens of potato. The potato resistance gene Ny<sub>tbr</sub> confers hypersensitive resistance to the ordinary strain of PVY (PVY<sup>O</sup>), but not the necrotic strain (PVY<sup>N</sup>). Here, we unveil that residue 247 of PVY helper component proteinase (HCPro) acts as a central player controlling Ny<sub>tbr</sub> strain-specific activation. We found that substituting the serine at 247 in the HCPro of PVY<sup>O</sup> (HCPro<sup>O</sup>) with an alanine as in PVY<sup>N</sup> HCPro (HCPro<sup>N</sup>) disrupts Ny<sub>tbr</sub> recognition. Conversely, an HCPro<sup>N</sup> mutant carrying a serine at position 247 triggers defence. Moreover, we demonstrate that plant defences are induced against HCPro<sup>O</sup> mutants with a phosphomimetic or another phosphorylatable residue at 247, but not with a phosphoablative residue, suggesting that phosphorylation could modulate Ny<sub>tbr</sub> resistance. Extending beyond PVY, we establish that the same response elicited by the PVY<sup>O</sup> HCPro is also induced by HCPro proteins from other members of the Potyviridae family that have a serine at position 247, but not by those with an alanine. Together, our results provide further insights in the strain-specific PVY resistance in potato and infer a broad-spectrum detection mechanism of plant potyvirus effectors contingent on a single amino acid residue.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 11","pages":"e70027"},"PeriodicalIF":4.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591341","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}
Caihong Liu, Karl-Heinz Kogel, Maria Ladera-Carmona
{"title":"Harnessing RNA interference for the control of Fusarium species: A critical review.","authors":"Caihong Liu, Karl-Heinz Kogel, Maria Ladera-Carmona","doi":"10.1111/mpp.70011","DOIUrl":"10.1111/mpp.70011","url":null,"abstract":"<p><p>Fusarium fungi are a pervasive threat to global agricultural productivity. They cause a spectrum of plant diseases that result in significant yield losses and threaten food safety by producing mycotoxins that are harmful to human and animal health. In recent years, the exploitation of the RNA interference (RNAi) mechanism has emerged as a promising avenue for the control of Fusarium-induced diseases, providing both a mechanistic understanding of Fusarium gene function and a potential strategy for environmentally sustainable disease management. However, despite significant progress in elucidating the presence and function of the RNAi pathway in different Fusarium species, a comprehensive understanding of its individual protein components and underlying silencing mechanisms remains elusive. Accordingly, while a considerable number of RNAi-based approaches to Fusarium control have been developed and many reports of RNAi applications in Fusarium control under laboratory conditions have been published, the applicability of this knowledge in agronomic settings remains an open question, and few convincing data on RNAi-based disease control under field conditions have been published. This review aims to consolidate the current knowledge on the role of RNAi in Fusarium disease control by evaluating current research and highlighting important avenues for future investigation.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70011"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372250","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}
Li-Juan Zhu, Yu Zhu, Chengwu Zou, Lan-Yi Su, Chong-Tao Zhang, Chi Wang, Ya-Ni Bai, Baoshan Chen, Rongbai Li, Qingfa Wu, Shou-Wei Ding, Jian-Guo Wu, Yan-Hong Han
{"title":"New persistent plant RNA virus carries mutations to weaken viral suppression of antiviral RNA interference.","authors":"Li-Juan Zhu, Yu Zhu, Chengwu Zou, Lan-Yi Su, Chong-Tao Zhang, Chi Wang, Ya-Ni Bai, Baoshan Chen, Rongbai Li, Qingfa Wu, Shou-Wei Ding, Jian-Guo Wu, Yan-Hong Han","doi":"10.1111/mpp.70020","DOIUrl":"10.1111/mpp.70020","url":null,"abstract":"<p><p>Persistent plant viruses are widespread in natural ecosystems. However, little is known about why persistent infection with these viruses may cause little or no harm to their host. Here, we discovered a new polerovirus that persistently infected wild rice plants by deep sequencing and assembly of virus-derived small-interfering RNAs (siRNAs). The new virus was named Rice tiller inhibition virus 2 (RTIV2) based on the symptoms developed in cultivated rice varieties following Agrobacterium-mediated inoculation with an infectious RTIV2 clone. We showed that RTIV2 infection induced antiviral RNA interference (RNAi) in both the wild and cultivated rice plants as well as Nicotiana benthamiana. It is known that virulent virus infection in plants depends on effective suppression of antiviral RNAi by viral suppressors of RNAi (VSRs). Notably, the P0 protein of RTIV2 exhibited weak VSR activity and carries alanine substitutions of two amino acids broadly conserved among diverse poleroviruses. Mixed infection with umbraviruses enhanced RTIV2 accumulation and/or enabled its mechanical transmission in N. benthamiana. Moreover, replacing the alanine at either one or both positions of RTIV2 P0 enhanced the VSR activity in a co-infiltration assay, and RTIV2 mutants carrying the corresponding substitutions replicated to significantly higher levels in both rice and N. benthamiana plants. Together, our findings show that as a persistent plant virus, RTIV2 carries specific mutations in its VSR gene to weaken viral suppression of antiviral RNAi. Our work reveals a new strategy for persistent viruses to maintain long-term infection by weak suppression of the host defence response.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70020"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11513406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504361","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}
{"title":"Autophagy plays an antiviral defence role against tomato spotted wilt orthotospovirus and is counteracted by viral effector NSs.","authors":"Xingwang Zhang, Hao Hong, Jiaoling Yan, Yulong Yuan, Mingfeng Feng, Qinhai Liu, Yanxiao Zhao, Tongqing Yang, Shen Huang, Chunli Wang, Ruizhen Zhao, Wenyu Zuo, Suyu Liu, Zixuan Ding, Changjun Huang, Zhongkai Zhang, Jiban Kumar Kundu, Xiaorong Tao","doi":"10.1111/mpp.70012","DOIUrl":"10.1111/mpp.70012","url":null,"abstract":"<p><p>Autophagy, an intracellular degradation process, has emerged as a crucial innate immune response against various plant pathogens, including viruses. Tomato spotted wilt orthotospovirus (TSWV) is a highly destructive plant pathogen that infects over 1000 plant species and poses a significant threat to global food security. However, the role of autophagy in defence against the TSWV pathogen, and whether the virus counteracts this defence, remains unknown. In this study, we report that autophagy plays an important role in antiviral defence against TSWV infection; however, this autophagy-mediated defence is counteracted by the viral effector NSs. Transcriptome profiling revealed the up-regulation of autophagy-related genes (ATGs) upon TSWV infection. Blocking autophagy induction by chemical treatment or knockout/down of ATG5/ATG7 significantly enhanced TSWV accumulation. Notably, the TSWV nucleocapsid (N) protein, a major component of the viral replication unit, strongly induced autophagy. However, the TSWV nonstructural protein NSs was able to effectively suppress N-induced autophagy in a dose-dependent manner. Further investigation revealed that NSs inhibited ATG6-mediated autophagy induction. These findings provide new insights into the defence role of autophagy against TSWV, a representative segmented negative-strand RNA virus, as well as the tospoviral pathogen counterdefence mechanism.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70012"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350330","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}
{"title":"Editing of the MeSWEET10a promoter yields bacterial blight resistance in cassava cultivar SC8.","authors":"Yajie Wang, Mengting Geng, Ranran Pan, Tong Zhang, Xiaohua Lu, Xinghou Zhen, Yannian Che, Ruimei Li, Jiao Liu, Yinhua Chen, Jianchun Guo, Yuan Yao","doi":"10.1111/mpp.70010","DOIUrl":"10.1111/mpp.70010","url":null,"abstract":"<p><p>Cassava starch is a widely used raw material for industrial production and food source for people. However, cassava bacterial blight (CBB) caused by Xanthomonas axonopodis pv. manihotis (Xam) results in severe yield losses and is the most destructive bacterial disease in all worldwide cassava-growing regions. Xam11 is a highly pathogenic subspecies from China that infects the Chinese local cassava South China No. 8 (SC8) cultivar with marked symptoms. This study showed that the transcription activator-like effector TALE20<sub>Xam11</sub> of Xam11 strain regulates the expression of disease-susceptibility gene MeSWEET10a by binding to the EBE<sub>TALE20</sub> region of the MeSWEET10a promoter in cassava cultivar SC8. CRISPR/Cas9-generated mutations of the EBE<sub>TALE20</sub> region resulted in a significant reduction in MeSWEET10a expression after infection by Xam11, correlating with reduced disease symptoms, smaller lesion sizes and decreased bacterial proliferation compared with the wild type. Importantly, the edited plants maintained normal growth, development and yield characteristics under greenhouse conditions. The results lay a research foundation for breeding resistant cassava cultivar SC8 to bacterial blight.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70010"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350331","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}
Qiuting Ren, Zhe Zhang, Yongle Zhang, Yue Zhang, Yujie Gao, Hongyi Zhang, Xianhong Wang, Guoping Wang, Ni Hong
{"title":"Protein P5 of pear chlorotic leaf spot-associated virus is a pathogenic factor that suppresses RNA silencing and enhances virus movement.","authors":"Qiuting Ren, Zhe Zhang, Yongle Zhang, Yue Zhang, Yujie Gao, Hongyi Zhang, Xianhong Wang, Guoping Wang, Ni Hong","doi":"10.1111/mpp.70015","DOIUrl":"https://doi.org/10.1111/mpp.70015","url":null,"abstract":"<p><p>Pear chlorotic leaf spot-associated virus (PCLSaV) is a newly described emaravirus that infects pear trees. The virus genome consists of at least five single-stranded, negative-sense RNAs. The P5 encoded by RNA5 is unique to PCLSaV. In this study, the RNA silencing suppression (RSS) activity of P5 and its subcellular localization were determined in Nicotiana benthamiana plants by Agrobacterium tumefaciens-mediated expression assays and green fluorescent protein RNA silencing induction. Protein P5 partially suppressed local RNA silencing, strongly suppressed systemic RNA silencing and triggered reactive oxygen species accumulation. The P5 self-interacted and showed subcellular locations in plasmodesmata, endoplasmic reticulum and nucleus. Furthermore, P5 rescued the cell-to-cell movement of a movement defective mutant PVXΔP25 of potato virus X (PVX) and enhanced the pathogenicity of PVX. The N-terminal 1-89 amino acids of the P5 were responsible for the self-interaction ability and RSS activity, for which the signal peptide at positions 1-19 was indispensable. This study demonstrated the function of an emaravirus protein as a pathogenic factor suppressing plant RNA silencing to enhance virus infection and as an enhancer of virus movement.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70015"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11481690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470155","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}
{"title":"Two plant membrane-shaping reticulon-like proteins play contrasting complex roles in turnip mosaic virus infection.","authors":"Guanwei Wu, Liping Wang, Rongrong He, Xiaoyan Cui, Xin Chen, Aiming Wang","doi":"10.1111/mpp.70017","DOIUrl":"https://doi.org/10.1111/mpp.70017","url":null,"abstract":"<p><p>Positive-sense RNA viruses remodel cellular cytoplasmic membranes as the membranous sources for the formation of viral replication organelles (VROs) for viral genome replication. In plants, they traffic through plasmodesmata (PD), plasma membrane-lined pores enabling cytoplasmic connections between cells for intercellular movement and systemic infection. In this study, we employed turnip mosaic virus (TuMV), a plant RNA virus to investigate the involvement of RTNLB3 and RTNLB6, two ER (endoplasmic reticulum) membrane-bending, PD-located reticulon-like (RTNL) non-metazoan group B proteins (RTNLBs) in viral infection. We show that RTNLB3 interacts with TuMV 6K2 integral membrane protein and RTNLB6 binds to TuMV coat protein (CP). Knockdown of RTNLB3 promoted viral infection, whereas downregulation of RTNLB6 restricted viral infection, suggesting that these two RTNLs play contrasting roles in TuMV infection. We further demonstrate that RTNLB3 targets the α-helix motif <sup>42</sup>LRKSM<sup>46</sup> of 6K2 to interrupt 6K2 self-interactions and compromise 6K2-induced VRO formation. Moreover, overexpression of AtRTNLB3 apparently promoted the selective degradation of the ER and ER-associated protein calnexin, but not 6K2. Intriguingly, mutation of the α-helix motif of 6K2 that is required for induction of VROs severely affected 6K2 stability and abolished TuMV infection. Thus, RTNLB3 attenuates TuMV replication, probably through the suppression of 6K2 function. We also show that RTNLB6 promotes viral intercellular movement but does not affect viral replication. Therefore, the proviral role of RTNLB6 is probably by enhancing viral cell-to-cell trafficking. Taken together, our data demonstrate that RTNL family proteins may play diverse complex, even opposite, roles in viral infection in plants.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70017"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11481689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470156","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}
{"title":"A virulent milRNA inhibits host immunity by silencing a host receptor-like kinase MaLYK3 and facilitates infection by Fusarium oxysporum f. sp. cubense.","authors":"Jiahui He, Jiaqi Zhong, Longqi Jin, Yike Long, Junjian Situ, Chengcheng He, Guanghui Kong, Zide Jiang, Minhui Li","doi":"10.1111/mpp.70016","DOIUrl":"10.1111/mpp.70016","url":null,"abstract":"<p><p>MicroRNA-like RNAs (milRNAs) play a significant role in the infection process by plant-pathogenic fungi. However, the specific functions and regulatory mechanisms of fungal milRNAs remain insufficiently elucidated. This study investigated the function of Foc-milR138, an infection-induced milRNA secreted by Fusarium oxysporum f. sp. cubense (Foc), which is the causal agent of Fusarium wilt of banana. Initially, through precursor gene knockout and phenotypic assessments, we confirmed that Foc-milR138 acts as a virulent milRNA prominently upregulated during the early stages of Foc infection. Subsequent bioinformatic analyses and transient expression assays in Nicotiana benthamiana leaves identified a host receptor-like kinase gene, MaLYK3, as the direct target of Foc-milR138. Functional investigations of MaLYK3 revealed its pivotal role in triggering immune responses of N. benthamiana by upregulating a suite of resistance genes, bolstering reactive oxygen species (ROS) accumulation and callose deposition, thereby fortifying disease resistance. This response was markedly subdued upon co-expression with Foc-milR138. Expression pattern analysis further verified the specific suppression of MaLYK3 by Foc-milR138 during the early root infection by Foc. In conclusion, Foc secretes a virulent milRNA (Foc-milR138) to enter the host banana cells and inhibit the expression of the plant surface receptor-like kinase MaLYK3, subverting the disease resistance activated by MaLYK3, and ultimately facilitating pathogen invasion. These findings shed light on the roles of fungal milRNAs and their targets in resistance and pathogenicity, offering promising avenues for the development of disease-resistant banana cultivars.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70016"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11470196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470152","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}
{"title":"Caffeic acid: A game changer in pine wood nematode overwintering survival.","authors":"Jianan Wang, Qiaoli Chen, Bihe Xu, Qi Yu, Yulan Shen, Hao Wu, Shengwei Jiang, Yantao Zhou, Danlei Li, Feng Wang","doi":"10.1111/mpp.70018","DOIUrl":"10.1111/mpp.70018","url":null,"abstract":"<p><p>Following the invasion by the pine wood nematode (PWN) into north-east China, a notable disparity in susceptibility was observed among Pinaceae species. Larix olgensis exhibited marked resilience and suffered minimal fatalities, while Pinus koraiensis experienced significant mortality due to PWN infection. Our research demonstrated that the PWNs in L. olgensis showed a 13.43% reduction in lipid content compared to P. koraiensis (p < 0.05), which was attributable to the accumulation of caffeic acid in L. olgensis. This reduction in lipid content was correlated with a decreased overwintering survival of PWNs. The diminished lipid reserves were associated with substantial stunting in PWNs, including reduced body length and maximum body width. The result suggests that lower lipid content is a major factor contributing to the lower overwintering survival rate of PWNs in L. olgensis induced by caffeic acid. Through verification tests, we concluded that the minimal fatalities observed in L. olgensis could be attributed to the reduced overwintering survival of PWNs, a consequence of caffeic acid-induced stunting. This study provides valuable insights into PWN-host interactions and suggests that targeting caffeic acid biosynthesis pathways could be a potential strategy for managing PWN in forest ecosystems.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70018"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11493755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470154","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}
{"title":"The perception and evolution of flagellin, cold shock protein and elongation factor Tu from vector-borne bacterial plant pathogens.","authors":"Jessica Trinh, Megann Tran, Gitta Coaker","doi":"10.1111/mpp.70019","DOIUrl":"10.1111/mpp.70019","url":null,"abstract":"<p><p>Vector-borne bacterial pathogens cause devastating plant diseases that cost billions of dollars in crop losses worldwide. These pathogens have evolved to be host- and vector-dependent, resulting in a reduced genome size compared to their free-living relatives. All known vector-borne bacterial plant pathogens belong to four different genera: 'Candidatus Liberibacter', 'Candidatus Phytoplasma', Spiroplasma and Xylella. To protect themselves against pathogens, plants have evolved pattern recognition receptors that can detect conserved pathogen features as non-self and mount an immune response. To gain an understanding of how vector-borne pathogen features are perceived in plants, we investigated three proteinaceous features derived from cold shock protein (csp22), flagellin (flg22) and elongation factor Tu (elf18) from vector-borne bacterial pathogens as well as their closest free-living relatives. In general, vector-borne pathogens have fewer copies of genes encoding flagellin and cold shock protein compared to their closest free-living relatives. Furthermore, epitopes from vector-borne pathogens were less likely to be immunogenic compared to their free-living counterparts. Most Liberibacter csp22 and elf18 epitopes do not trigger plant immune responses in tomato or Arabidopsis. Interestingly, csp22 from the citrus pathogen 'Candidatus Liberibacter asiaticus' triggers immune responses in solanaceous plants, while csp22 from the solanaceous pathogen 'Candidatus Liberibacter solanacearum' does not. Our findings suggest that vector-borne plant pathogenic bacteria evolved to evade host recognition.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e70019"},"PeriodicalIF":4.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11512079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504362","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}