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The Moniliophthora roreri Effector MrB1 Affects Cellular Homeostasis and Induces Genotype-Dependent Necrosis in Theobroma cacao. 霉霉效应物MrB1影响可可细胞稳态并诱导基因型依赖性坏死。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70316

Taís Araújo Santos, Maria Luíza do Carmo Santos, Monaliza Macêdo Ferreira, Keilane Silva Farias, Carlos Henrique de Carvalho Neto, Ronan Xavier Corrêa, Uilson Vanderlei Lopes, Carlos Priminho Pirovani

{"title":"The Moniliophthora roreri Effector MrB1 Affects Cellular Homeostasis and Induces Genotype-Dependent Necrosis in Theobroma cacao.","authors":"Taís Araújo Santos, Maria Luíza do Carmo Santos, Monaliza Macêdo Ferreira, Keilane Silva Farias, Carlos Henrique de Carvalho Neto, Ronan Xavier Corrêa, Uilson Vanderlei Lopes, Carlos Priminho Pirovani","doi":"10.1111/mpp.70316","DOIUrl":"10.1111/mpp.70316","url":null,"abstract":"<p><p>Frosty pod rot (FPR) is an invasive disease responsible for severe yield losses of cacao trees. In this study, we characterised the MrB1 protein (BASIDIN1 from Moniliophthora roreri), a homologue of the BASIDIN effector protein from M. perniciosa. Recombinant MrB1 (rMrB1) induced morphological changes typical of necrosis in Nicotiana benthamiana cell suspensions, including cell swelling, reduced GFP (green fluorescent protein) fluorescence, plasma membrane damage, and electrolyte leakage. Proteomic analysis of the cells indicated that rMrB1 treatment modulated proteins associated with cellular homeostasis, including reduced abundance of proteins related to energy metabolism and protein folding, such as BiP (Binding Immunoglobulin Protein), whose non-detection was validated by western blotting. In cacao leaves, spraying with rMrB1 (12.5 μM) resulted in necrotic lesions affecting 54% of the leaf area after 10 days, increasing to 77% in the presence of 0.5% urea. At a lower concentration (5 μM), the recombinant protein promoted hydrogen peroxide accumulation, supporting the induction of oxidative stress. The phenotypic response to rMrB1 varied among cacao genotypes with different levels of resistance to FPR and witches' broom disease, with the susceptible Catongo genotype being the most affected, while resistant genotypes, such as ICS-95 and Scavina-6, did not show visible symptoms. These results position MrB1 among the few functionally characterised effector proteins in the M. roreri-Theobroma cacao pathosystem and suggest that this effector may be further evaluated as a candidate marker of susceptibility in cacao breeding programmes.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70316"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430669","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

Silencing Suppressor Protein p26 of Areca Palm Velarivirus 1 (APV1) Interacts With SGS3 and Promotes Its Degradation Via the Ubiquitination Pathway. 槟榔棕榈病毒1 （APV1）沉默抑制蛋白p26与SGS3相互作用并通过泛素化途径促进其降解。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70303

Xianmei Cao, Yutian Wang, Li Zhang, Yongqi Liang, Jiping Zheng, Hongxing Wang, Ruibai Zhao, Xi Huang

{"title":"Silencing Suppressor Protein p26 of Areca Palm Velarivirus 1 (APV1) Interacts With SGS3 and Promotes Its Degradation Via the Ubiquitination Pathway.","authors":"Xianmei Cao, Yutian Wang, Li Zhang, Yongqi Liang, Jiping Zheng, Hongxing Wang, Ruibai Zhao, Xi Huang","doi":"10.1111/mpp.70303","DOIUrl":"10.1111/mpp.70303","url":null,"abstract":"<p><p>RNA silencing is a conserved defence mechanism against viral infections in eukaryotes, whereas many plant viruses evolved viral suppressors of RNA silencing (VSRs) to counteract the antiviral silencing in hosts. Areca palm velarivirus 1 (APV1), a member of genus Velarivirus, family Closteroviridae, is a causal agent of yellow leaf disease affecting Areca catechu in Hainan, China. In this work, we identified the APV1-encoded p26 protein as a multifunctional VSR that suppresses local silencing induced by single-stranded RNA (ssRNA), systemic silencing induced by ssRNA and double-stranded RNA (dsRNA), and the systemic spread of silencing signals. p26 was shown to be a viral pathogenicity factor that enhances the accumulation and pathogenicity of recombinant potato virus X (PVX). The suppressor of gene silencing 3 protein of A. catechu (AcSGS3), a key component of the plant antiviral silencing pathway, was proved to be a host factor interacting with p26. Both APV1 infection and p26 overexpression significantly induced NbSGS3 expression in Nicotiana benthamiana. The accumulation level of AcSGS3 protein decreased in the presence of p26, and such degradation was sensitive to the ubiquitination inhibitor MG132. Overexpression of p26 disturbed the interaction between SGS3 and the RNA-dependent RNA polymerase 6 protein (RDR6), another key component coordinating with SGS3 in antiviral silencing. Our study reveals the molecular mechanism of p26-mediated suppression of host antiviral defence by targeting SGS3 for accelerated degradation via the ubiquitination pathway.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70303"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422505","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

Canonical ETI-Dependent and -Independent Pathways Mediate Autoimmunity Caused by Loss of CBP60b Clade Function. 典型的eti依赖性和非依赖性通路介导CBP60b进化枝功能丧失引起的自身免疫。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70318

Lu-Shen Li, Yan-Yan Yang, Lin Ma, Shu-Lei Wang, Sha Li

{"title":"Canonical ETI-Dependent and -Independent Pathways Mediate Autoimmunity Caused by Loss of CBP60b Clade Function.","authors":"Lu-Shen Li, Yan-Yan Yang, Lin Ma, Shu-Lei Wang, Sha Li","doi":"10.1111/mpp.70318","DOIUrl":"10.1111/mpp.70318","url":null,"abstract":"<p><p>Calmodulin-Binding Protein 60 (CBP60), a plant-specific atypical transcription factor family, plays pivotal roles in reprogramming plant immunity. Loss of function of the CBP60b and CBP60b/c/d/e/f subfamily constitutively activates immune responses (autoimmunity). However, the specific mechanisms and pathways underlying this autoimmunity remain elusive. Here, through EMS mutagenesis of the cbp60b mutant, we isolated a dominant suppressor mutant that suppresses the cbp60b autoimmune phenotype. Sequencing identified a point mutation in CBP60g (designated cbp60g-3) that causes an aspartate-to-asparagine substitution at position 252 and reduces its transcriptional activity. Increasing the expression of CBP60g<sup>D252N</sup> restored the pathogen response defect of the cbp60g;sard1 mutant. Strikingly, while wild-type CBP60g failed to suppress the autoimmunity of cbp60b, the transcriptionally compromised CBP60g<sup>D252N</sup> variant completely suppressed it. Unexpectedly, we found that functional loss of canonical effector-triggered immunity (ETI) pathways only partially suppressed the autoimmunity of the cbp60b;c;d;e;f quintuple mutant. Although simultaneously disrupting the ETI pathways and introducing CBP60g<sup>D252N</sup> further suppressed the autoimmunity of cbp60b;c;d;e;f, it still failed to achieve complete suppression. These results indicate that the autoimmunity in cbp60b;c;d;e;f mutant is mediated by both canonical ETI-dependent and ETI-independent pathways. These results provide new insights and raise further questions regarding the signalling mechanisms of plant autoimmunity.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70318"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13354941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422527","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

Imprecise Cas12a/ssODN-Mediated Editing of eIF4E1 Confers Dominant-Negative Resistance to Potato Virus Y in Solanum tuberosum. 不精确的Cas12a/ ssodn介导的eIF4E1编辑赋予茄对马铃薯Y病毒的显性负抗性

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70305

Alessandra Lucioli, Raffaela Tavazza, Attila Molnar, Vincenza Ilardi, Adéla Přibylová, Mario Tavazza

{"title":"Imprecise Cas12a/ssODN-Mediated Editing of eIF4E1 Confers Dominant-Negative Resistance to Potato Virus Y in Solanum tuberosum.","authors":"Alessandra Lucioli, Raffaela Tavazza, Attila Molnar, Vincenza Ilardi, Adéla Přibylová, Mario Tavazza","doi":"10.1111/mpp.70305","DOIUrl":"10.1111/mpp.70305","url":null,"abstract":"<p><p>Mutants in the eukaryotic initiation factor 4E (eIF4E) gene family provide recessive resistance to plant viruses. Previously, we demonstrated that knocking out SteIF4E1 potato alleles (A, B, B, B1) resulted in limited resistance to a necrogenic PVY isolate (NTN). Expanding on this, we used a non-transgenic method employing Cas12a and a single-stranded oligodeoxynucleotide (ssODN) as a repair template to introduce amino acid changes in SteIF4E1, attempting to mimic the Capsicum PVY resistance allele pvr2<sup>1</sup>. However, no plants that had been regenerated from transfected protoplast cells displayed correct SteIF4E1 editing. Instead, truncated sequence duplications (pvr2<sup>1</sup>SD) appeared at some mutated alleles, suggesting that ssODN-mediated repair predominantly occurs via microhomology-mediated end joining. Importantly, out of the 39 edited lines tested, the dwarf line Bb29 exhibited resistance to PVY-NTN and showed reduced systemic infection sustained by PVY-O. Notably, PVY-NTN resistance-breaking isolates occasionally emerged in Bb29, confirming genuine eIF4E-mediated resistance. In Bb29, three of four eIF4E1 copies were mutated (AΔ12, BΔ6, B, B1pvr2<sup>1</sup>SD), with SteIF4E1_B1pvr2<sup>1</sup>SD featuring a premature stop codon at the 5' end of the mutated sequence, and the unique SteIF4E1_AΔ12 allele in our gene-edited lines. We found that SteIF4E1_BΔ6, but not SteIF4E1_AΔ12, partially complemented an eIF4E-deficient yeast strain. In addition, introducing a wild-type copy of SteIF4E1 into Bb29 restored virus susceptibility and partially reversed dwarfism. Conversely, transforming wild-type potatoes with SteIF4E1_AΔ12 mimicked the resistance profile of Bb29, conferring stronger and broader resistance against PVY than the SteIF4E1 knockout approach. These findings reveal a dominant-negative resistance mechanism, opening new avenues for engineering potyvirus resistance.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70305"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13315812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352526","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

FgCot1 Regulates Polarized Growth and Conidiation in Fusarium graminearum via Gpmk1 MAPK and Tsf1 Transcriptional Pathways. FgCot1通过Gpmk1、MAPK和Tsf1转录途径调控稻瘟病菌的极化生长和条件作用。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70321

Chengliang Li, Shaozhe Qin, Daiyuan Sun, Jingyi Ren, Cong Jiang, Jin-Rong Xu, Guanghui Wang

{"title":"FgCot1 Regulates Polarized Growth and Conidiation in Fusarium graminearum via Gpmk1 MAPK and Tsf1 Transcriptional Pathways.","authors":"Chengliang Li, Shaozhe Qin, Daiyuan Sun, Jingyi Ren, Cong Jiang, Jin-Rong Xu, Guanghui Wang","doi":"10.1111/mpp.70321","DOIUrl":"10.1111/mpp.70321","url":null,"abstract":"<p><p>Fusarium graminearum causes Fusarium head blight (FHB), a devastating wheat disease that threatens global food security and safety. Nuclear Dbf2-related (NDR) kinases regulate cellular morphogenesis, but their roles in phytopathogenic fungi remain elusive. Here, we characterized F. graminearum NDR kinase FgCot1, whose deletion severely disrupted vegetative growth, conidiation, polarized growth and pathogenicity. Notably, the Fgcot1 mutant showed genetic instability, producing fast-growing suppressors with primary (Gpmk1 pathway genes), secondary (MFS transporter SSF1) and tertiary (transcription factor TSF1) mutations. Functional analyses revealed that disrupting the Gpmk1 pathway partially rescued the Fgcot1 growth defects due to Gpmk1 hyperactivation, whereas SSF1 deletion independently enhanced growth. The TSF1<sup>R386C</sup> mutation suppressed the Fgcot1 growth defect via a Gpmk1/Ssf1-independent pathway. Moreover, FST11 deletion and TSF1<sup>R386C</sup> mutation significantly alleviated the Fgcot1 mutant's polarized growth defect and slightly restored conidiation, suggesting that Gpmk1 and Tsf1 function in parallel pathways downstream of FgCot1 kinase. Finally, we demonstrated that FgCot1 interacts with Tsf1 and regulates its protein stability and nuclear accumulation; R386C mutation restored these defects of Tsf1 in the Fgcot1 mutant. Collectively, FgCot1 kinase integrates Gpmk1 signalling and Tsf1-dependent transcription to govern polarized growth and conidiation in F. graminearum.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70321"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579466","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 Transcription Factor DPB Confers Antiviral Defence Against Potato Virus X by Modulating MYB-Dependent Signalling. 转录因子DPB通过调节myb依赖性信号传导赋予马铃薯病毒X抗病毒防御

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70319

Jingjing Shi, Yumei Zhao, Chunyan Qi, Yaoyao Jiang, Bin Yong, Lingyun Lei, Wenhao Wang, Peng Liu, Jiaqian Liu, Tianye Zhang, Jianping Chen, Jian Yang, Tianbo Liu, Kaili Zhong

{"title":"The Transcription Factor DPB Confers Antiviral Defence Against Potato Virus X by Modulating MYB-Dependent Signalling.","authors":"Jingjing Shi, Yumei Zhao, Chunyan Qi, Yaoyao Jiang, Bin Yong, Lingyun Lei, Wenhao Wang, Peng Liu, Jiaqian Liu, Tianye Zhang, Jianping Chen, Jian Yang, Tianbo Liu, Kaili Zhong","doi":"10.1111/mpp.70319","DOIUrl":"10.1111/mpp.70319","url":null,"abstract":"<p><p>As a transcriptional co-factor of E2F, DP proteins are typically involved in the regulation of plant cell-cycle-related processes. However, whether DP proteins participate in transcriptional regulation associated with plant antiviral defence remains largely unclear. This study demonstrates that NbDPB, a DP family protein in Nicotiana benthamiana, positively regulates resistance to potato virus X (PVX) by functioning as a transcription factor. Knockout of NbDPB increased plant susceptibility to PVX, while its overexpression significantly suppressed viral accumulation. Furthermore, we identified that NbDPB binds to the promoter of NbMYB (a MYB transcription factor) and positively regulates its expression. Silencing NbMYB enhanced PVX infection, whereas exogenous application of jasmonic acid (JA) and salicylic acid (SA) partially rescued this phenotype. Hormone levels of JA and SA, as well as the expression levels of their marker genes, were significantly reduced in the silenced NbMYB plants. These findings suggest that the NbDPB-NbMYB module mediates antiviral defence through the JA and SA signalling pathways. This study reveals a previously uncharacterized role of DP proteins in antiviral transcriptional regulation, indicating that they may play a crucial role in plant antiviral defence.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70319"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430690","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

Alternative Polyadenylation Dynamics During the Rice Blast Immune Response. 水稻稻瘟病免疫应答过程中的选择性聚腺苷酸化动力学。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70301

Dewei Yang, Xinyi Li, Haohua He, Niqing He, Qingshun Q Li, Haihui Fu

{"title":"Alternative Polyadenylation Dynamics During the Rice Blast Immune Response.","authors":"Dewei Yang, Xinyi Li, Haohua He, Niqing He, Qingshun Q Li, Haihui Fu","doi":"10.1111/mpp.70301","DOIUrl":"10.1111/mpp.70301","url":null,"abstract":"<p><p>Alternative polyadenylation (APA) is a widespread post-transcriptional regulation that generates transcripts with variable 3' untranslated region (UTR) lengths. In this study, poly(A)-tag sequencing (PAT-seq) was performed during the process of Magnaporthe oryzae infection of rice. Genome-wide dynamic changes of APA profiles were identified during the response, with widespread shortening of gene transcripts. Shortened genes were found to function in biological processes associated with stress responses. Importantly, the changes of 3' UTR length were negatively related to the expression levels of the corresponding genes. In addition, we found that the expression levels of miRNAs that bind to the 3' UTRs of the APA genes were negatively correlated with the expression levels of the corresponding APA genes. This correlation suggests a potential regulatory strategy where immune-related genes might evade miRNA-mediated repression via 3' UTR shortening. To assess the biological impact of these APA dynamics, we functionally characterised a representative candidate, Os05g0509500, that exhibits complex and dynamic APA site switching upon infection. Knockout of Os05g0509500 via CRISPR/Cas9 revealed its positive regulatory role in rice blast, offering initial insights into the function of APA in this disease. Several core polyadenylation protein factors were significantly differentially expressed during the rice response. Our results revealed that the precise transcriptome-wide poly(A) site selection of genes during rice blast challenge, and the relationships between miRNAs and targeted APA genes, are tightly regulated. Such a mechanism provides a new perspective for designing novel strategies to control rice blast disease.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70301"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13305335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331179","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

Late Blight Effector Pi05910 Suppresses Plant Immunity by Promoting Destabilisation of Host Scaffold Protein RACK1. 晚疫病效应物Pi05910通过促进宿主支架蛋白RACK1的失稳抑制植物免疫。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70311

Xiong Liu, Yisa Wang, Song Liu, Xiran Li, Liwen Ding, Altyn Shayakhmetova, Yuling Meng, Weixing Shan

{"title":"Late Blight Effector Pi05910 Suppresses Plant Immunity by Promoting Destabilisation of Host Scaffold Protein RACK1.","authors":"Xiong Liu, Yisa Wang, Song Liu, Xiran Li, Liwen Ding, Altyn Shayakhmetova, Yuling Meng, Weixing Shan","doi":"10.1111/mpp.70311","DOIUrl":"10.1111/mpp.70311","url":null,"abstract":"<p><p>Late blight, caused by oomycete pathogen Phytophthora infestans, is one of the most devastating diseases of potato and tomato. Plant resistance to pathogens relies on a sophisticated innate immune system, which is often targeted by pathogen-derived effectors. P. infestans secretes numerous RXLR effectors to suppress host immunity. In this study, we show that the P. infestans core effector Pi05910 functions as a virulence factor and targets the host scaffold protein Receptor for Activated C Kinase 1 (RACK1), which is identified to positively regulate potato resistance to late blight. Functional analyses showed that StRACK1-silencing in potato, and tobacco rattle virus (TRV)-based virus-induced NbRACK1-silencing in Nicotiana benthamiana, consistently increased host susceptibility to P. infestans colonisation, whereas transient expression of NbRACK1 in N. benthamiana or stable overexpression of StRACK1 in potato enhanced late blight resistance. Pi05910 physically interacts with RACK1 and promotes its destabilisation via the host 26S proteasome pathway. The destabilisation of RACK1 led to the inhibition of PAMP elicitor INF1-triggered plant immune responses, including reactive oxygen species burst and expression of defence-related genes such as StWRKY7 and StWRKY8, and suppression of potato and N. benthamiana growth and global protein translation. Our findings reveal a strategy whereby a pathogen effector sabotages a key potato immune scaffold StRACK1 to promote plant susceptibility to P. infestans infection, providing new insight into mechanisms of effector-triggered plant susceptibility.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70311"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382314","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

Puccinia triticina Effector Pt3863 Targets and Subverts TaRLCK176 to Suppress Wheat Resistance to Leaf Rust. 小麦锈病效应物Pt3863靶向并破坏TaRLCK176抑制小麦对叶锈病的抗性

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70317

Jiaojie Zhao, Weishuai Bi, Na Zhang, Na Li, Xuefeng Fan, Hao Li, Lulu Song, Yue Qi, Johannes Mapuranga, Tongjun Sun, Wenxiang Yang

{"title":"Puccinia triticina Effector Pt3863 Targets and Subverts TaRLCK176 to Suppress Wheat Resistance to Leaf Rust.","authors":"Jiaojie Zhao, Weishuai Bi, Na Zhang, Na Li, Xuefeng Fan, Hao Li, Lulu Song, Yue Qi, Johannes Mapuranga, Tongjun Sun, Wenxiang Yang","doi":"10.1111/mpp.70317","DOIUrl":"10.1111/mpp.70317","url":null,"abstract":"<p><p>Wheat leaf rust, caused by Puccinia triticina, is a widespread economically important wheat disease. During infection, P. triticina secretes effectors proteins to manipulate host immunity. Here we identified and characterized the P. triticina effector Pt3863, which is highly expressed during the early phase of infection and significantly enhances fungal virulence. We also identified the wheat receptor-like cytoplasmic kinase TaRLCK176 as a target of Pt3863. Functional assays demonstrated that TaRLCK176 positively regulates wheat resistance against leaf rust and is required for chitin-induced reactive oxygen species (ROS) accumulation. Pt3863 subverts this defence through a dual inhibitory mechanism: first, it suppresses TaRLCK176 phosphorylation; second, it promotes TaRLCK176 degradation via the ubiquitin-26S proteasome pathway. Host-induced gene silencing Pt3863 attenuated P. triticina virulence, while its overexpression in transgenic wheat lines increased susceptibility to P. tritici. Conversely, virus-induced gene silencing of TaRLCK176 compromised wheat resistance. Our findings establish TaRLCK176 as a critical immune hub that positively modulates wheat resistance to leaf rust and is specifically targeted by the P. triticina effector Pt3863. Notably, Pt3863 has evolved a sophisticated virulence strategy to simultaneously disrupt both the phosphorylation-mediated activation and proteasomal stability of TaRLCK176, thereby impairing host immune responses. This study elucidates a key molecular mechanism underlying the suppression of wheat immunity by P. triticina and highlights TaRLCK176 as a promising candidate target for the genetic engineering of durable resistance in wheat against leaf rust.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70317"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520777","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

Phytoplasma Effector SJP8 Suppresses Host Immunity by Promoting the Degradation of ZjMYB15 and ZjMYB86-like to Perturb Jasmonic Acid and Hydrogen Peroxide Homeostasis in Jujube. 植物原体效应物SJP8通过促进ZjMYB15和ZjMYB86-like降解扰乱枣中茉莉酸和过氧化氢的稳态来抑制宿主免疫。

IF 5 1区农林科学

Molecular plant pathology Pub Date : 2026-07-01 DOI: 10.1111/mpp.70315

Ying Yang, Haizhen Nie, Weikai Chen, Yaru Xu, Bo Wu, Ling Ma, Zhonghua Liu, Xiaoming Pang

{"title":"Phytoplasma Effector SJP8 Suppresses Host Immunity by Promoting the Degradation of ZjMYB15 and ZjMYB86-like to Perturb Jasmonic Acid and Hydrogen Peroxide Homeostasis in Jujube.","authors":"Ying Yang, Haizhen Nie, Weikai Chen, Yaru Xu, Bo Wu, Ling Ma, Zhonghua Liu, Xiaoming Pang","doi":"10.1111/mpp.70315","DOIUrl":"10.1111/mpp.70315","url":null,"abstract":"<p><p>'Candidatus Phytoplasma ziziphi' infection causes severe damage to jujube (Ziziphus jujuba), inducing symptoms such as branch clustering, dwarfism, chlorosis and phyllody, leading to significant economic losses. However, the pathogenic mechanisms underlying jujube witches'-broom (JWB) disease remain largely unknown. In this study, we identified SJP8 as a key secreted effector protein of 'Ca. P. ziziphi'. Overexpression of SJP8 in jujube recapitulated the characteristic JWB-like symptoms, including dwarfism and leaf chlorosis. Transcriptome analysis revealed that SJP8 suppressed host immunity by downregulating jasmonic acid (JA)-related genes and upregulating hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-related genes. SJP8 interacts with ZjMYB15 and ZjMYB86-like and promotes their degradation via the 26S proteasome pathway. Genetic transformation experiments demonstrated that ZjMYB15 and ZjMYB86-like positively regulate plant height and the expression of JA-related genes while repressing H<sub>2</sub>O<sub>2</sub>-associated genes. ZjMYB15 and ZjMYB86-like bind to their cognate motifs to activate ZjJAIPHX1 (encoding a jasmonate-induced protein homologue isoform X1) and ZjPOD43 (encoding peroxidase 43) transcription, thereby increasing JA content and decreasing H<sub>2</sub>O<sub>2</sub> levels. Collectively, these results establish that the SJP8-ZjMYB15/ZjMYB86-like-ZjJAIPHX1/ZjPOD43 module suppresses plant immunity by perturbing JA and H<sub>2</sub>O<sub>2</sub> homeostasis, thus both elucidating a phytoplasma effector's virulence strategy and providing molecular targets for breeding resistant jujube.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"27 7","pages":"e70315"},"PeriodicalIF":5.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422502","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}

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