Gayal (Bos frontalis) an endangered bovine species inhabitingChina, India, Bangladesh, Myanmar and Bhutan, has a mysterious evolutionary origin. Shaped by natural selection, its unique traits make it a valuable genetic resource; however, its populations are rapidly declining. In this study, comprehensive whole-genome resequencing of fifty-eight samples of Gayal from China, India, Myanmar and Bangladesh was performed. We identified over 44 million SNPs across four Gayal populations. Nucleotide diversity analysis revealed variations in genetic diversity, with the lowest occurring in India and the highest occurring in China. Phylogenetic tree analysis revealed three distinct clades representing China, India and Bangladesh-Myanmar, which were further confirmed by principal component and admixture analyses. The genetic exchanges between Gayal and other bovine species indicate limited influence from domestic cattle in both the Chinese and Bangladeshi Gayal populations. Mitochondrial DNA sequences and a phylogenetic tree highlighted the unique mitochondrial genome of Gayal. Genome-wide selection signals pinpointed candidate genes linked to mitochondrial function, immunity, musculoskeletal development, reproduction and growth performance. Distinct haplotype patterns emerged for the CCDC157, KIAA0753 and MTFP1 genes in the Chinese and Bangladesh-Myanmar Gayal populations, indicating artificial selection in the Chinese population. KEGG pathway and gene ontology enrichment analyses provided insights into processes related to neurodevelopment, cardiac function, tissue growth, immunity and metabolism. In summary, our study enhances our understanding of Gayal genetics, population structure and selection signals across four countries. This knowledge is crucial for conserving this endangered species amid its rapid decline.
{"title":"Evaluation of genetic diversity and selection signals in gayal populations across four countries through whole-genome resequencing.","authors":"Xin Liu, Qiaoxian Li, Jianyong Liu, Zulfiqar Ahmed, Jicai Zhang, Zhe Wang, Ankui Wang, Ningbo Chen, Yongzhen Huang, Gang Ren, Hong Chen, Chuzhao Lei, Bizhi Huang","doi":"10.1007/s44154-025-00252-7","DOIUrl":"10.1007/s44154-025-00252-7","url":null,"abstract":"<p><p>Gayal (Bos frontalis) an endangered bovine species inhabitingChina, India, Bangladesh, Myanmar and Bhutan, has a mysterious evolutionary origin. Shaped by natural selection, its unique traits make it a valuable genetic resource; however, its populations are rapidly declining. In this study, comprehensive whole-genome resequencing of fifty-eight samples of Gayal from China, India, Myanmar and Bangladesh was performed. We identified over 44 million SNPs across four Gayal populations. Nucleotide diversity analysis revealed variations in genetic diversity, with the lowest occurring in India and the highest occurring in China. Phylogenetic tree analysis revealed three distinct clades representing China, India and Bangladesh-Myanmar, which were further confirmed by principal component and admixture analyses. The genetic exchanges between Gayal and other bovine species indicate limited influence from domestic cattle in both the Chinese and Bangladeshi Gayal populations. Mitochondrial DNA sequences and a phylogenetic tree highlighted the unique mitochondrial genome of Gayal. Genome-wide selection signals pinpointed candidate genes linked to mitochondrial function, immunity, musculoskeletal development, reproduction and growth performance. Distinct haplotype patterns emerged for the CCDC157, KIAA0753 and MTFP1 genes in the Chinese and Bangladesh-Myanmar Gayal populations, indicating artificial selection in the Chinese population. KEGG pathway and gene ontology enrichment analyses provided insights into processes related to neurodevelopment, cardiac function, tissue growth, immunity and metabolism. In summary, our study enhances our understanding of Gayal genetics, population structure and selection signals across four countries. This knowledge is crucial for conserving this endangered species amid its rapid decline.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"61"},"PeriodicalIF":5.8,"publicationDate":"2025-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12553695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145370509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-26DOI: 10.1007/s44154-025-00265-2
Kun Wang, Yaqin Wang, Shuai Fu, Yuchong Tan, Liang Wu, Yi Xu, Jianxiang Wu, Xueping Zhou
Modification of proteins by ubiquitin is a dynamic and reversible process. It is unclear whether rice stripe virus (RSV) can modulate the plant deubiquitination pathway. In this study, we found that RSV infection can specifically upregulate the expression of the deubiquitinase NbUBP16. Further analysis revealed that NbUBP16 stabilizes serine hydroxymethyltrasferase (SHMT1) by binding to NbSHMT1 and removing its polyubiquitination modification mediated by E3 ligase MEL, which inhibits downstream SHMT1-mediated ROS accumulation and thereby facilitates RSV infection. Our findings provide new insights into the molecular arms race between pathogens and plants, demonstrating how a plant virus can undermine plant defenses by hijacking host deubiquitination pathways.
{"title":"Upregulation of deubiquitinase UBP16 induced by rice stripe virus infection stabilizes SHMT1 to suppress ROS accumulation and facilitate virus infection in Nicotiana benthamiana.","authors":"Kun Wang, Yaqin Wang, Shuai Fu, Yuchong Tan, Liang Wu, Yi Xu, Jianxiang Wu, Xueping Zhou","doi":"10.1007/s44154-025-00265-2","DOIUrl":"10.1007/s44154-025-00265-2","url":null,"abstract":"<p><p>Modification of proteins by ubiquitin is a dynamic and reversible process. It is unclear whether rice stripe virus (RSV) can modulate the plant deubiquitination pathway. In this study, we found that RSV infection can specifically upregulate the expression of the deubiquitinase NbUBP16. Further analysis revealed that NbUBP16 stabilizes serine hydroxymethyltrasferase (SHMT1) by binding to NbSHMT1 and removing its polyubiquitination modification mediated by E3 ligase MEL, which inhibits downstream SHMT1-mediated ROS accumulation and thereby facilitates RSV infection. Our findings provide new insights into the molecular arms race between pathogens and plants, demonstrating how a plant virus can undermine plant defenses by hijacking host deubiquitination pathways.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"62"},"PeriodicalIF":5.8,"publicationDate":"2025-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12553715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145370513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-16DOI: 10.1007/s44154-025-00231-y
George Bawa, Yang Shen, Mingzhe Sun, Xiaoli Sun
As a barrier between the cell and its environment, the plant cell wall provides structural support during development and stress response. Plants are able to sense their surroundings and adjust their activities accordingly. A crucial mechanism involved in these adaptive changes is the cell wall integrity (CWI) maintenance mechanism, which monitors and maintains the integrity of cell walls via changes in cell and cell wall metabolism without destroying cell wall organization. Different abiotic stresses and changes in plant developmental phases disrupt CWI. However, emerging evidence has demonstrated the initiation of CWI signaling mechanisms as key in promoting plant growth in complex situations. This review discusses recent advances in the Catharanthus roseus receptor-like kinase 1-like (CrRLK1L) protein function in plant cell wall signaling during adaptation to changing environments and development. We conclude by highlighting how current spatially resolved transcriptomics may be used to advance the role of CrRLK1L members in plant cell wall signaling during development and stress response.
{"title":"Advances in CrRLK1L function in plant cell wall signaling during interaction with the environment and development.","authors":"George Bawa, Yang Shen, Mingzhe Sun, Xiaoli Sun","doi":"10.1007/s44154-025-00231-y","DOIUrl":"10.1007/s44154-025-00231-y","url":null,"abstract":"<p><p>As a barrier between the cell and its environment, the plant cell wall provides structural support during development and stress response. Plants are able to sense their surroundings and adjust their activities accordingly. A crucial mechanism involved in these adaptive changes is the cell wall integrity (CWI) maintenance mechanism, which monitors and maintains the integrity of cell walls via changes in cell and cell wall metabolism without destroying cell wall organization. Different abiotic stresses and changes in plant developmental phases disrupt CWI. However, emerging evidence has demonstrated the initiation of CWI signaling mechanisms as key in promoting plant growth in complex situations. This review discusses recent advances in the Catharanthus roseus receptor-like kinase 1-like (CrRLK1L) protein function in plant cell wall signaling during adaptation to changing environments and development. We conclude by highlighting how current spatially resolved transcriptomics may be used to advance the role of CrRLK1L members in plant cell wall signaling during development and stress response.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"60"},"PeriodicalIF":5.8,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12532557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145304926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-13DOI: 10.1007/s44154-025-00266-1
Qingqing Hou, Xuewei Chen
Sheath blight (ShB), caused by the necrotrophic fungus Rhizoctonia solani, is a globally destructive rice disease responsible for significant yield losses. However, the absence of characterized genes conferring high potential resistance to sheath blight within natural rice germplasm constrains resistance breeding. A recent study published in Nature Genetics uncovered the ShB resistance receptor-like kinase 1 (SBRR1) as a key gene associated with disease resistance. SBRR1-R, an elite resistance allele mainly presented in indica rice and distinguished by a 256-bp promoter insertion, confers strong resistance without obvious yield penalty. SBRR1 is the first gene with major effects underlying natural variation in sheath blight resistance, offering significant potential for rice breeding. Furthermore, the discovery of the "bHLH57-SBRR1-R-SIP1-Chit3/4" defense module provides fundamental insights into rice immunity and a molecular module with substantial breeding potential.
{"title":"Rice breeding against sheath blight is now feasible: a breakthrough discovery of SBRR1-mediated sheath blight resistance from natural rice germplasm.","authors":"Qingqing Hou, Xuewei Chen","doi":"10.1007/s44154-025-00266-1","DOIUrl":"10.1007/s44154-025-00266-1","url":null,"abstract":"<p><p>Sheath blight (ShB), caused by the necrotrophic fungus Rhizoctonia solani, is a globally destructive rice disease responsible for significant yield losses. However, the absence of characterized genes conferring high potential resistance to sheath blight within natural rice germplasm constrains resistance breeding. A recent study published in Nature Genetics uncovered the ShB resistance receptor-like kinase 1 (SBRR1) as a key gene associated with disease resistance. SBRR1-R, an elite resistance allele mainly presented in indica rice and distinguished by a 256-bp promoter insertion, confers strong resistance without obvious yield penalty. SBRR1 is the first gene with major effects underlying natural variation in sheath blight resistance, offering significant potential for rice breeding. Furthermore, the discovery of the \"bHLH57-SBRR1-R-SIP1-Chit3/4\" defense module provides fundamental insights into rice immunity and a molecular module with substantial breeding potential.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"59"},"PeriodicalIF":5.8,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-16DOI: 10.1007/s44154-025-00233-w
Tamana Khan, Labiba Shah, Sabba Khan, Owais Ali Wani, Zahid Nabi Sheikh, Baseerat Afroza, Rizwan Rashid, Faheem Shahzad Baloch, Sheikh Mansoor
Heavy metal pollution severely impacts plant health by inhibiting growth, photosynthesis, enzyme activities, and causing oxidative stress. Plants respond to such stress by activating complex defense mechanisms involving reactive oxygen species and different signaling pathways. These pathways are pivotal in triggering plant defense responses and are currently a major focus of research. Understanding the complex mechanisms of heavy metal uptake, transport, chelation, and signaling can guide strategies to improve plant resilience and stress tolerance. In this review, we aim to highlight the key heavy metals found in soil and the environment, along with their mechanisms of accumulation in plants. We also explore the defense responses of plants through various signaling pathways such as calcium (Ca2+), MAP kinase, and hormone signaling. Additionally, we emphasize the importance of understanding advanced omics technologies, including transcriptomics, metabolomics, and bioinformatic tools, in enhancing our knowledge of plant resilience and stress tolerance.
{"title":"Comprehensive review of multiomics applications and remediation of plant heavy metal toxicity.","authors":"Tamana Khan, Labiba Shah, Sabba Khan, Owais Ali Wani, Zahid Nabi Sheikh, Baseerat Afroza, Rizwan Rashid, Faheem Shahzad Baloch, Sheikh Mansoor","doi":"10.1007/s44154-025-00233-w","DOIUrl":"10.1007/s44154-025-00233-w","url":null,"abstract":"<p><p>Heavy metal pollution severely impacts plant health by inhibiting growth, photosynthesis, enzyme activities, and causing oxidative stress. Plants respond to such stress by activating complex defense mechanisms involving reactive oxygen species and different signaling pathways. These pathways are pivotal in triggering plant defense responses and are currently a major focus of research. Understanding the complex mechanisms of heavy metal uptake, transport, chelation, and signaling can guide strategies to improve plant resilience and stress tolerance. In this review, we aim to highlight the key heavy metals found in soil and the environment, along with their mechanisms of accumulation in plants. We also explore the defense responses of plants through various signaling pathways such as calcium (Ca<sup>2+</sup>), MAP kinase, and hormone signaling. Additionally, we emphasize the importance of understanding advanced omics technologies, including transcriptomics, metabolomics, and bioinformatic tools, in enhancing our knowledge of plant resilience and stress tolerance.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"58"},"PeriodicalIF":5.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Plant cells exhibit an extraordinary regenerative potential, achieving cellular totipotency by dedifferentiating to form new tissues. While significant progress has been made in understanding cell fate mechanisms, the regulatory networks governing callus cell development remain insufficiently explored, particularly regarding cell classification, morphology, and regulatory processes. This study provides a detailed investigation into the developmental dynamics and transcriptomic profiles of callus cells in Arabidopsis at key stages: initiation, proliferation, and greening. Employing single-cell RNA sequencing and UMAP-based clustering, we annotated cell clusters based on highly enriched gene expressions. Developmental trajectories were further mapped through pseudotime analysis, revealing distinct transcription factor networks. Additionally, functional analysis of key regulatory genes was conducted using mutant and overexpression lines, affirming their roles in callus development. Gene Ontology analysis highlighted the involvement of environmental factors-low oxygen and salinity promoted callus formation, while light inhibited it, though essential for greening. These findings shed light on the complex regulatory landscape of plant tissue regeneration and guide future research avenues.
{"title":"Single-cell RNA sequencing reveals developmental trajectories and environmental regulation of callus formation in Arabidopsis.","authors":"Zhixin Liu, Yixin Zhang, Qianli Zhao, Hao Liu, Yaping Zhou, Aizhi Qin, Chunyang Li, Lulu Yan, Mengfan Li, Peibo Gao, Xiao Song, Yajie Xie, Enzhi Guo, Luyao Kong, Liping Guan, Guoyong An, Xuwu Sun","doi":"10.1007/s44154-025-00255-4","DOIUrl":"10.1007/s44154-025-00255-4","url":null,"abstract":"<p><p>Plant cells exhibit an extraordinary regenerative potential, achieving cellular totipotency by dedifferentiating to form new tissues. While significant progress has been made in understanding cell fate mechanisms, the regulatory networks governing callus cell development remain insufficiently explored, particularly regarding cell classification, morphology, and regulatory processes. This study provides a detailed investigation into the developmental dynamics and transcriptomic profiles of callus cells in Arabidopsis at key stages: initiation, proliferation, and greening. Employing single-cell RNA sequencing and UMAP-based clustering, we annotated cell clusters based on highly enriched gene expressions. Developmental trajectories were further mapped through pseudotime analysis, revealing distinct transcription factor networks. Additionally, functional analysis of key regulatory genes was conducted using mutant and overexpression lines, affirming their roles in callus development. Gene Ontology analysis highlighted the involvement of environmental factors-low oxygen and salinity promoted callus formation, while light inhibited it, though essential for greening. These findings shed light on the complex regulatory landscape of plant tissue regeneration and guide future research avenues.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"57"},"PeriodicalIF":5.8,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12431987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-09DOI: 10.1007/s44154-025-00254-5
Jianqing Zhao, Weiwei Yao, Qingqing Liu, Ping Gong, Yuanpan Mu, Wei Wang, Baolong Liu, Cong Li, Hengbo Shi, Jun Luo
Understanding the genetic mechanism of cold adaptation in cashmere goats and dairy goats is very important to improve their production performance. The purpose of this study was to comprehensively analyze the genetic basis of goat adaptation to cold environments, clarify the impact of environmental factors on genome diversity, and lay the foundation for breeding goat breeds to adapt to climate change. A total of 240 dairy goats were subjected to genome resequencing, and the whole genome sequencing data of 57 individuals from 6 published breeds were incorporated. By integrating multiple approaches such as phylogenetic analysis, population structure analysis, gene flow and population history exploration, selection signal analysis, and genome-environment association analysis, an in-depth investigation was carried out. Phylogenetic analysis unraveled the genetic relationships and differentiation patterns among dairy goats and other goat breeds. Through signal analysis (θπ, FST, XP-CLR), we identified numerous candidate genes associated with cold adaptation in dairy goats (STRIP1, ALX3, HTR4, NTRK2, MRPL11, PELI3, DPP3, BBS1) and cashmere goats (MED12L, MARC2, MARC1, DSG3, C6H4orf22, CHD7, MYPN, KIAA0825, MITF). Genome-environment association (GEA) analysis confirmed the link between these genes and environmental factors. Moreover, a detailed analysis of the critical genes C6H4orf22 and STRIP1 demonstrated their significant roles in the geographical variations of cold adaptation and allele frequency differences among different breeds. This study contributes to understanding the genetic basis of cold adaptation, providing crucial theoretical support for precision breeding programs aimed at improving production performance in cold regions by leveraging adaptive alleles, thereby ensuring sustainable animal husbandry.
{"title":"Landscape genomics analysis reveals the genetic basis underlying cashmere goats and dairy goats adaptation to frigid environments.","authors":"Jianqing Zhao, Weiwei Yao, Qingqing Liu, Ping Gong, Yuanpan Mu, Wei Wang, Baolong Liu, Cong Li, Hengbo Shi, Jun Luo","doi":"10.1007/s44154-025-00254-5","DOIUrl":"10.1007/s44154-025-00254-5","url":null,"abstract":"<p><p>Understanding the genetic mechanism of cold adaptation in cashmere goats and dairy goats is very important to improve their production performance. The purpose of this study was to comprehensively analyze the genetic basis of goat adaptation to cold environments, clarify the impact of environmental factors on genome diversity, and lay the foundation for breeding goat breeds to adapt to climate change. A total of 240 dairy goats were subjected to genome resequencing, and the whole genome sequencing data of 57 individuals from 6 published breeds were incorporated. By integrating multiple approaches such as phylogenetic analysis, population structure analysis, gene flow and population history exploration, selection signal analysis, and genome-environment association analysis, an in-depth investigation was carried out. Phylogenetic analysis unraveled the genetic relationships and differentiation patterns among dairy goats and other goat breeds. Through signal analysis (θπ, FST, XP-CLR), we identified numerous candidate genes associated with cold adaptation in dairy goats (STRIP1, ALX3, HTR4, NTRK2, MRPL11, PELI3, DPP3, BBS1) and cashmere goats (MED12L, MARC2, MARC1, DSG3, C6H4orf22, CHD7, MYPN, KIAA0825, MITF). Genome-environment association (GEA) analysis confirmed the link between these genes and environmental factors. Moreover, a detailed analysis of the critical genes C6H4orf22 and STRIP1 demonstrated their significant roles in the geographical variations of cold adaptation and allele frequency differences among different breeds. This study contributes to understanding the genetic basis of cold adaptation, providing crucial theoretical support for precision breeding programs aimed at improving production performance in cold regions by leveraging adaptive alleles, thereby ensuring sustainable animal husbandry.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"56"},"PeriodicalIF":5.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145024900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nucleotide-binding leucine-rich repeat (NLR) proteins assemble into genetically linked pairs to mediate effector-triggered immunity (ETI) in plants. Here, we characterize the paired NLRs NRCX and NARY (NRCX adjacent resistance gene Y) in Nicotiana benthamiana. CRISPR/Cas9 knockout of NRCX caused severe dwarfism and constitutively activated immunity, marked by PR1 upregulation and enhanced resistance to Phytophthora capsici. Co-silencing or double knockout of the adjacent NLR NARY partially rescued the nrcx phenotype, revealing NARY as a compensatory regulator that modulates growth and immunity. Structural analysis revealed that NARY harbors non-canonical Walker B and MHD motifs, which lack autoactivation capacity despite their divergence from canonical NLR executors. Split-luciferase and co-immunoprecipitation assays showed that NRCX and NARY interact exclusively through their CC domains, forming a non-canonical regulatory complex. Notably, simultaneous silencing of NRC2/3 and NARY incompletely restored growth in nrcx mutants, implicating additional factors in immune modulation. Our findings establish NARY as a compensatory NLR partner of NRCX that fine-tunes immunity without triggering cell death, revealing a novel mechanism for balancing growth and defense in Solanaceae.
{"title":"A CNL protein forms an NLR pair with NRCX to modulate plant immunity.","authors":"Xiaohua Dong, Xiaoyan Zhang, Xu Lu, Yufeng Yang, Chuyan Xia, Weiye Pan, Zhiyuan Yin, Yaning Zhao, Gan Ai, Daolong Dou","doi":"10.1007/s44154-025-00245-6","DOIUrl":"10.1007/s44154-025-00245-6","url":null,"abstract":"<p><p>Nucleotide-binding leucine-rich repeat (NLR) proteins assemble into genetically linked pairs to mediate effector-triggered immunity (ETI) in plants. Here, we characterize the paired NLRs NRCX and NARY (NRCX adjacent resistance gene Y) in Nicotiana benthamiana. CRISPR/Cas9 knockout of NRCX caused severe dwarfism and constitutively activated immunity, marked by PR1 upregulation and enhanced resistance to Phytophthora capsici. Co-silencing or double knockout of the adjacent NLR NARY partially rescued the nrcx phenotype, revealing NARY as a compensatory regulator that modulates growth and immunity. Structural analysis revealed that NARY harbors non-canonical Walker B and MHD motifs, which lack autoactivation capacity despite their divergence from canonical NLR executors. Split-luciferase and co-immunoprecipitation assays showed that NRCX and NARY interact exclusively through their CC domains, forming a non-canonical regulatory complex. Notably, simultaneous silencing of NRC2/3 and NARY incompletely restored growth in nrcx mutants, implicating additional factors in immune modulation. Our findings establish NARY as a compensatory NLR partner of NRCX that fine-tunes immunity without triggering cell death, revealing a novel mechanism for balancing growth and defense in Solanaceae.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"55"},"PeriodicalIF":5.8,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12405136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environmental stress adaptation is crucial for the survival and pathogenicity of plant fungal pathogens. In this study, we identified a transcription factor FgMsn2 in Fusarium graminearum, an ortholog of Msn2 in budding yeast. Structural analysis showed that the C2H2 zinc-finger domain is highly conserved across fungi, while other regions are less conserved, suggesting that FgMsn2 may have species-specific functions. Subsequently, we revealed that FgMsn2 is critical for vegetative growth, and conidiogenesis. Deletion of FgMSN2 severely reduced the deoxynivalenol (DON) production and pathogenicity, while enhancing tolerance to oxidative, osmotic, cell wall and membrane stresses. Furthermore, our RNA-seq analysis revealed that FgMsn2 regulates genes involved in energy metabolism, lipid metabolism and stress responses, emphasizing its role in maintaining metabolic balance and stress adaptability. Notably, FgMsn2 influences mitochondrial morphology, as the Fgmsn2 mutant exhibited disrupted mitochondrial structures and reduced ATP production. The Fgmsn2 mutant also showed increased lipid droplet accumulation, indicating the FgMsn2's role in lipid metabolism. Taken together, the FgMsn2 serves as a key regulator in fungal development, plant infection, stress responses, and metabolism. Our study provides valuable insights into the molecular mechanisms of fungal stress adaptation and pathogenicity, suggesting a potential target for the development of more effective fungicides and disease management strategies.
{"title":"FgMsn2, a zinc finger transcription factor, regulates stress responses, pathogenicity and metabolism in wheat scab fungus Fusarium graminearum.","authors":"Daiyuan Sun, Chengliang Li, Liangyuan Zhao, Jinling Yang, Haijuan Li, Kaili Duan, Chenfang Wang, Guanghui Wang","doi":"10.1007/s44154-025-00249-2","DOIUrl":"10.1007/s44154-025-00249-2","url":null,"abstract":"<p><p>Environmental stress adaptation is crucial for the survival and pathogenicity of plant fungal pathogens. In this study, we identified a transcription factor FgMsn2 in Fusarium graminearum, an ortholog of Msn2 in budding yeast. Structural analysis showed that the C2H2 zinc-finger domain is highly conserved across fungi, while other regions are less conserved, suggesting that FgMsn2 may have species-specific functions. Subsequently, we revealed that FgMsn2 is critical for vegetative growth, and conidiogenesis. Deletion of FgMSN2 severely reduced the deoxynivalenol (DON) production and pathogenicity, while enhancing tolerance to oxidative, osmotic, cell wall and membrane stresses. Furthermore, our RNA-seq analysis revealed that FgMsn2 regulates genes involved in energy metabolism, lipid metabolism and stress responses, emphasizing its role in maintaining metabolic balance and stress adaptability. Notably, FgMsn2 influences mitochondrial morphology, as the Fgmsn2 mutant exhibited disrupted mitochondrial structures and reduced ATP production. The Fgmsn2 mutant also showed increased lipid droplet accumulation, indicating the FgMsn2's role in lipid metabolism. Taken together, the FgMsn2 serves as a key regulator in fungal development, plant infection, stress responses, and metabolism. Our study provides valuable insights into the molecular mechanisms of fungal stress adaptation and pathogenicity, suggesting a potential target for the development of more effective fungicides and disease management strategies.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"54"},"PeriodicalIF":5.8,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12401790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cucumber target spot, a major disease that threatens cucumber production, is caused by Corynespora cassiicola. Cyclobutrifluram, a novel succinate dehydrogenase inhibitor (SDHI) developed by Syngenta, has demonstrated strong inhibitory activity against various plant pathogenic fungi and nematodes. However, its antifungal spectrum, resistance risk as well as underlying mechanisms of resistance in C. cassiicola remain poorly understood. In this study, cyclobutrifluram exhibited potent inhibitory activity against anamorphic fungi and selected ascomycetes, with the mean sensitivity of C. cassiicola isolates to the fungicide being 0.98 ± 1.26 μg/mL. Additionally, five laboratory-derived cyclobutrifluram-resistant mutants showed comparable or lower biological fitness than their respective parental isolates. The resistant mutants and field isolates were also found to possess nine distinct point mutations in the CcSdhB, CcSdhC or CcSdhD genes. Finally, cyclobutrifluram exhibited positive cross-resistance with other SDHIs, with the resistance levels varying depending on the specific mutations present. In conclusion, cyclobutrifluram was found to be effective against anamorphic fungi and selected ascomycetes. C. cassiicola's risk of resistance development to cyclobutrifluram was assessed as moderate to high and was primarily associated with mutations in CcSdh genes.
{"title":"Antifungal spectrum of cyclobutrifluram and multi-point mutations in CcSdh proteins confer resistance in Corynespora cassiicola.","authors":"Xinchang Hao, Yiwen Li, Zhaoyue Hang, Yue Chen, Yidong Tang, Jianqiang Miao, Qin Peng, Xili Liu","doi":"10.1007/s44154-025-00251-8","DOIUrl":"10.1007/s44154-025-00251-8","url":null,"abstract":"<p><p>Cucumber target spot, a major disease that threatens cucumber production, is caused by Corynespora cassiicola. Cyclobutrifluram, a novel succinate dehydrogenase inhibitor (SDHI) developed by Syngenta, has demonstrated strong inhibitory activity against various plant pathogenic fungi and nematodes. However, its antifungal spectrum, resistance risk as well as underlying mechanisms of resistance in C. cassiicola remain poorly understood. In this study, cyclobutrifluram exhibited potent inhibitory activity against anamorphic fungi and selected ascomycetes, with the mean sensitivity of C. cassiicola isolates to the fungicide being 0.98 ± 1.26 μg/mL. Additionally, five laboratory-derived cyclobutrifluram-resistant mutants showed comparable or lower biological fitness than their respective parental isolates. The resistant mutants and field isolates were also found to possess nine distinct point mutations in the CcSdhB, CcSdhC or CcSdhD genes. Finally, cyclobutrifluram exhibited positive cross-resistance with other SDHIs, with the resistance levels varying depending on the specific mutations present. In conclusion, cyclobutrifluram was found to be effective against anamorphic fungi and selected ascomycetes. C. cassiicola's risk of resistance development to cyclobutrifluram was assessed as moderate to high and was primarily associated with mutations in CcSdh genes.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"5 1","pages":"53"},"PeriodicalIF":5.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12399480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}