Fusarium graminearum, the causal agent of Fusarium head blight (FHB), poses a major threat to global food security by contaminating cereals with the mycotoxin deoxynivalenol (DON). Although transcriptional and protein-level regulation of its stress response and virulence has been extensively studied, the functional significance of mRNA processing in these critical processes remains largely unexplored. Here, we identify Lsm8, a highly conserved core subunit of the nuclear Lsm2-8 complex, as a pivotal regulator linking RNA splicing fidelity to fungal growth, stress adaptation, and virulence. Deletion of LSM8 disrupted Lsm2-8 assembly and nuclear localization, resulting in widespread intron retention in genes essential for stress signaling (HOG1, ATF1), development (GPA1, STE12), and trichothecene biosynthesis. Consequently, osmoadaptation was impaired, sexual reproduction was abolished, and both DON production and virulence were drastically reduced. We further demonstrate that intron-retained transcripts are predominantly degraded by the RNA exosome, revealing a conserved Lsm8-exosome module that maintains splicing fidelity and RNA surveillance. Given the deep evolutionary conservation of Lsm8 across eukaryotes, these findings uncover a fundamental post-transcriptional regulatory layer governing fungal stress response, virulence, and mycotoxin biosynthesis, and highlight RNA-processing factors as universal determinants of virulence and promising antifungal targets across eukaryotic pathogens.
镰刀菌(Fusarium graminearum)是导致赤霉病(Fusarium head blight, FHB)的病原菌,它通过用真菌毒素脱氧雪腐镰刀菌醇(脱氧雪腐镰刀菌醇)污染谷物,对全球粮食安全构成重大威胁。尽管对其应激反应和毒力的转录和蛋白水平调控已经进行了广泛的研究,但mRNA加工在这些关键过程中的功能意义仍未被广泛探索。在这里,我们鉴定出Lsm8,核Lsm2-8复合体的一个高度保守的核心亚基,作为一个关键的调节因子,将RNA剪接保真度与真菌生长、胁迫适应和毒力联系起来。LSM8的缺失破坏了Lsm2-8的组装和核定位,导致在胁迫信号(HOG1, ATF1)、发育(GPA1, STE12)和毛藻生物合成所必需的基因中广泛保留内含子。因此,渗透适应被破坏,有性生殖被废除,DON的产生和毒力都大大降低。我们进一步证明内含子保留转录本主要被RNA外泌体降解,揭示了一个保守的lsm8外泌体模块,该模块维持剪接保真度和RNA监视。鉴于Lsm8在真核生物中的深度进化保守性,这些发现揭示了控制真菌胁迫反应、毒力和真菌毒素生物合成的基本转录后调控层,并强调了rna加工因子是真核病原体毒力的普遍决定因素和有希望的抗真菌靶点。
{"title":"A conserved Lsm8-exosome module maintains RNA splicing fidelity to control fungal stress adaptation and virulence.","authors":"Yiyi Ren, Haolan Cheng, Xingmin Han, Meiling Guo, Chenghui Xu, Jiayue Yan, Zhiwei Ge, Zhonghua Ma, Yun Chen","doi":"10.1007/s44154-026-00285-6","DOIUrl":"https://doi.org/10.1007/s44154-026-00285-6","url":null,"abstract":"<p><p>Fusarium graminearum, the causal agent of Fusarium head blight (FHB), poses a major threat to global food security by contaminating cereals with the mycotoxin deoxynivalenol (DON). Although transcriptional and protein-level regulation of its stress response and virulence has been extensively studied, the functional significance of mRNA processing in these critical processes remains largely unexplored. Here, we identify Lsm8, a highly conserved core subunit of the nuclear Lsm2-8 complex, as a pivotal regulator linking RNA splicing fidelity to fungal growth, stress adaptation, and virulence. Deletion of LSM8 disrupted Lsm2-8 assembly and nuclear localization, resulting in widespread intron retention in genes essential for stress signaling (HOG1, ATF1), development (GPA1, STE12), and trichothecene biosynthesis. Consequently, osmoadaptation was impaired, sexual reproduction was abolished, and both DON production and virulence were drastically reduced. We further demonstrate that intron-retained transcripts are predominantly degraded by the RNA exosome, revealing a conserved Lsm8-exosome module that maintains splicing fidelity and RNA surveillance. Given the deep evolutionary conservation of Lsm8 across eukaryotes, these findings uncover a fundamental post-transcriptional regulatory layer governing fungal stress response, virulence, and mycotoxin biosynthesis, and highlight RNA-processing factors as universal determinants of virulence and promising antifungal targets across eukaryotic pathogens.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"14"},"PeriodicalIF":5.8,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-10DOI: 10.1007/s44154-026-00288-3
Ruifeng Guo, Yicheng Li, Chen Tang, Yize Zhao, Mohan Wang, Guanghang Qiao, Steven J Klosterman, Yonglin Wang
Verticillium wilt, caused by the soilborne fungus Verticillium dahliae, has resulted in high mortality of Cotinus coggygria (smoke tree) in China. Symptoms of this disease are complex, many infected smoke trees exhibit wilting or dieback on some branches but no other branches. Whether other microbial taxa act synergistically to contribute to symptom development is unknown. Here, we investigated the microbial community assembly features associated with different branches of smoke trees with or without Verticillium wilt symptoms and established linkages between symptomatic branches and putative keystone taxa. Amplicon data analyses revealed that V. dahliae significantly affected the microbiota structure within tree branches. Microbial network connectivity indicated that Verticillium wilt destabilized the network, and fungal communities were more sensitive to Verticillium wilt than the bacterial communities. Based on taxonomic level information, the fungus Botryosphaeria dothidea was significantly enriched in diseased branches and positively correlated with the abundance of V. dahliae. Through microbial isolations, pathogen co-inoculations, histopathological assays, and RNA-seq analyses, the results indicated that plants infected with V. dahliae showed significantly increased susceptibility to B. dothidea and downregulated expression of defense-related genes. Overall, the results revealed that Verticillium wilt provokes changes in the structure of the smoke tree microbiome and that these changes likely influence symptom development in some but not all tree branches. The synergistic interplay between the commensal fungus B. dothidea and the soil-borne fungus V. dahliae promotes wilt progression in smoke trees, offering new insights into developing effective control strategies through fungicides plus enhancing host vigor.
{"title":"The bark latent fungus Botryosphaeria dothidea exacerbates branch dieback following the infection with Verticillium dahliae.","authors":"Ruifeng Guo, Yicheng Li, Chen Tang, Yize Zhao, Mohan Wang, Guanghang Qiao, Steven J Klosterman, Yonglin Wang","doi":"10.1007/s44154-026-00288-3","DOIUrl":"https://doi.org/10.1007/s44154-026-00288-3","url":null,"abstract":"<p><p>Verticillium wilt, caused by the soilborne fungus Verticillium dahliae, has resulted in high mortality of Cotinus coggygria (smoke tree) in China. Symptoms of this disease are complex, many infected smoke trees exhibit wilting or dieback on some branches but no other branches. Whether other microbial taxa act synergistically to contribute to symptom development is unknown. Here, we investigated the microbial community assembly features associated with different branches of smoke trees with or without Verticillium wilt symptoms and established linkages between symptomatic branches and putative keystone taxa. Amplicon data analyses revealed that V. dahliae significantly affected the microbiota structure within tree branches. Microbial network connectivity indicated that Verticillium wilt destabilized the network, and fungal communities were more sensitive to Verticillium wilt than the bacterial communities. Based on taxonomic level information, the fungus Botryosphaeria dothidea was significantly enriched in diseased branches and positively correlated with the abundance of V. dahliae. Through microbial isolations, pathogen co-inoculations, histopathological assays, and RNA-seq analyses, the results indicated that plants infected with V. dahliae showed significantly increased susceptibility to B. dothidea and downregulated expression of defense-related genes. Overall, the results revealed that Verticillium wilt provokes changes in the structure of the smoke tree microbiome and that these changes likely influence symptom development in some but not all tree branches. The synergistic interplay between the commensal fungus B. dothidea and the soil-borne fungus V. dahliae promotes wilt progression in smoke trees, offering new insights into developing effective control strategies through fungicides plus enhancing host vigor.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"13"},"PeriodicalIF":5.8,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-09DOI: 10.1007/s44154-025-00283-0
Heng Zhang, Guojun Feng, Yaozu Feng
Quinoa (Chenopodium quinoa Willd.), a semi-domesticated halophyte originating in the Andean region, has emerged as a promising crop for exploiting marginal lands, valued for its exceptional nutritional profile and remarkable resilience to high salinity and drought. This review analyzes the current status and future potential of quinoa as a model halophytic crop. We begin by examining the physiological mechanisms that enable quinoa to thrive in marginal environments, which have been the subject of extensive study. Thanks to the advancement in high-throughput sequencing technology, genomic resources - including the recent development of high-quality reference genomes and a Chenopodium pangenome - are rapidly expanding. Sequence-based genetic mapping techniques hold the promise to dissect the molecular basis of complex traits in combination with the utility of functional genomics tools such as virus-induced gene silencing (VIGS) and stable genetic transformation. Ultimately, the application of modern breeding technologies, such as phenomics, genomic selection (GS), and CRISPR/Cas, will expedite the development of locally adapted, climate-resilient quinoa cultivars worldwide.
{"title":"Quinoa as a naturally stress-resistant crop: current status and future promises.","authors":"Heng Zhang, Guojun Feng, Yaozu Feng","doi":"10.1007/s44154-025-00283-0","DOIUrl":"10.1007/s44154-025-00283-0","url":null,"abstract":"<p><p>Quinoa (Chenopodium quinoa Willd.), a semi-domesticated halophyte originating in the Andean region, has emerged as a promising crop for exploiting marginal lands, valued for its exceptional nutritional profile and remarkable resilience to high salinity and drought. This review analyzes the current status and future potential of quinoa as a model halophytic crop. We begin by examining the physiological mechanisms that enable quinoa to thrive in marginal environments, which have been the subject of extensive study. Thanks to the advancement in high-throughput sequencing technology, genomic resources - including the recent development of high-quality reference genomes and a Chenopodium pangenome - are rapidly expanding. Sequence-based genetic mapping techniques hold the promise to dissect the molecular basis of complex traits in combination with the utility of functional genomics tools such as virus-induced gene silencing (VIGS) and stable genetic transformation. Ultimately, the application of modern breeding technologies, such as phenomics, genomic selection (GS), and CRISPR/Cas, will expedite the development of locally adapted, climate-resilient quinoa cultivars worldwide.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"12"},"PeriodicalIF":5.8,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146144926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-06DOI: 10.1007/s44154-026-00293-6
Qiaoling Wang, Xingying Yan, Li Huang, Qi Niu, Ming Luo, Fan Xu
Sphingolipids are not only essential structural components of cellular membranes but also key signaling molecules that regulate plant growth, development, and stress responses. However, their specific roles in root development remain largely unknown. In the presented study, we demonstrate that overexpression of the GhGCS1 gene significantly enhances lateral root development in cotton. Integrated comprehensive transcriptome analysis and phytohormone quantification revealed that GhGCS1 promotes lateral root initiation and elongation primarily by suppressing cytokinin biosynthesis. Notably, GhGCS1 overexpression also markedly improved cotton resistance to Verticillium dahliae. Further molecular analyses indicated that GhGCS1 enhances cotton verticillium wilt resistance through modulation of the expression of sphingolipid-associated brassinosteroid- and pathogenesis-related genes. Collectively, these findings reveal a dual regulatory role for GhGCS1 in coordinating root architecture and immune responses in cotton, providing novel insights and potential strategies for developing crop varieties with improved yield potential and stress tolerance.
{"title":"Synergistic role of GhGCS1 in cotton root development and verticillium wilt resistance.","authors":"Qiaoling Wang, Xingying Yan, Li Huang, Qi Niu, Ming Luo, Fan Xu","doi":"10.1007/s44154-026-00293-6","DOIUrl":"10.1007/s44154-026-00293-6","url":null,"abstract":"<p><p>Sphingolipids are not only essential structural components of cellular membranes but also key signaling molecules that regulate plant growth, development, and stress responses. However, their specific roles in root development remain largely unknown. In the presented study, we demonstrate that overexpression of the GhGCS1 gene significantly enhances lateral root development in cotton. Integrated comprehensive transcriptome analysis and phytohormone quantification revealed that GhGCS1 promotes lateral root initiation and elongation primarily by suppressing cytokinin biosynthesis. Notably, GhGCS1 overexpression also markedly improved cotton resistance to Verticillium dahliae. Further molecular analyses indicated that GhGCS1 enhances cotton verticillium wilt resistance through modulation of the expression of sphingolipid-associated brassinosteroid- and pathogenesis-related genes. Collectively, these findings reveal a dual regulatory role for GhGCS1 in coordinating root architecture and immune responses in cotton, providing novel insights and potential strategies for developing crop varieties with improved yield potential and stress tolerance.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"11"},"PeriodicalIF":5.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12881189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133695","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 : 2026-01-29DOI: 10.1007/s44154-025-00267-0
Huanzhang Shang, Bo Ji, Thérèse Ouellet, Guangwei Li, Boliao Li, Xiulin Chen, Kun Luo
Indole-3-acetic acid (IAA) is a major naturally occurring auxin that shows extensive accumulation in cereal plants during the first few days of infection by the phytopathogen Fusarium graminearum. Apart from its positive effects on plant growth, empirical studies have suggested that it is a virulence factor that alters the host's nutritional level and fine-tunes the plant's immune responses, especially salicylic acid-mediated defenses. Plant and fungus genomic studies have predicted that their genomes carry the required genes for L-tryptophan-dependent IAA biosynthetic pathways. In recent decades, genetic and genomic studies have facilitated the description of L-tryptophan (L-TRP)-dependent IAA biosynthetic pathways in F. graminearum and its host plants. The present review illustrates and summarizes the putative and preference molecular networks related to extensive IAA accumulation in wheat heads triggered by infection with F. graminearum, based on the available knowledge about the endogenous IAA biosynthetic pathways in F. graminearum and wheat plants. Meanwhile, infection by F. graminearum could preferentially trigger L-TRP's conversion into serotonin and even phytomelatonin via tryptamine in wheat heads as well. Lower concentrations of them have been shown to stimulate IAA accumulation or mimic IAA to promote plant growth. However, upon that hardly provides sufficient information for regarding alternative methods of controlling scab epidemics. In combination with dissecting IAA biosynthetic pathways using genetic approaches exhibits many difficulties, we thus highlight that ongoing efforts should focus more on identifying the fungal effectors involved in extensive IAA accumulation in cereals in order to understand their potential roles in wheat-F. graminearum interactions. Advancements in molecular breeding programs will further accelerate the application of these molecular targets, allowing for the development of more scab-resistant wheat cultivars and resulting in the effective and environmentally friendly suppression of scab epidemics.
{"title":"Auxin accumulation in cereals after infection by Fusarium graminearum: putative biosynthetic pathways and preferences.","authors":"Huanzhang Shang, Bo Ji, Thérèse Ouellet, Guangwei Li, Boliao Li, Xiulin Chen, Kun Luo","doi":"10.1007/s44154-025-00267-0","DOIUrl":"10.1007/s44154-025-00267-0","url":null,"abstract":"<p><p>Indole-3-acetic acid (IAA) is a major naturally occurring auxin that shows extensive accumulation in cereal plants during the first few days of infection by the phytopathogen Fusarium graminearum. Apart from its positive effects on plant growth, empirical studies have suggested that it is a virulence factor that alters the host's nutritional level and fine-tunes the plant's immune responses, especially salicylic acid-mediated defenses. Plant and fungus genomic studies have predicted that their genomes carry the required genes for L-tryptophan-dependent IAA biosynthetic pathways. In recent decades, genetic and genomic studies have facilitated the description of L-tryptophan (L-TRP)-dependent IAA biosynthetic pathways in F. graminearum and its host plants. The present review illustrates and summarizes the putative and preference molecular networks related to extensive IAA accumulation in wheat heads triggered by infection with F. graminearum, based on the available knowledge about the endogenous IAA biosynthetic pathways in F. graminearum and wheat plants. Meanwhile, infection by F. graminearum could preferentially trigger L-TRP's conversion into serotonin and even phytomelatonin via tryptamine in wheat heads as well. Lower concentrations of them have been shown to stimulate IAA accumulation or mimic IAA to promote plant growth. However, upon that hardly provides sufficient information for regarding alternative methods of controlling scab epidemics. In combination with dissecting IAA biosynthetic pathways using genetic approaches exhibits many difficulties, we thus highlight that ongoing efforts should focus more on identifying the fungal effectors involved in extensive IAA accumulation in cereals in order to understand their potential roles in wheat-F. graminearum interactions. Advancements in molecular breeding programs will further accelerate the application of these molecular targets, allowing for the development of more scab-resistant wheat cultivars and resulting in the effective and environmentally friendly suppression of scab epidemics.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"10"},"PeriodicalIF":5.8,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12855686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146088088","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 viruses are among the most significant biotic stressors, posing a severe threat to crop productivity and global food security. Their success largely depends on the exploitation of host eukaryotic translation factors (eTFs), including initiation factors (eIFs) and elongation factors (eEFs), which act as molecular gatekeepers of the viral life cycle. Key members such as eIF4E, eIF(iso)4E, eIF4G, eEF1A, and eEF1B have been identified as susceptibility factors that mediate viral translation, replication, and systemic movement. Viruses have co-evolved specialized proteins and RNA elements, including VPg and IRES structures, to hijack these host factors and circumvent plant defense barriers. This review synthesizes current understanding of the mechanistic roles of eTFs in virus-host dynamics and highlights strategies to mitigate viral stress. Approaches such as natural allele mining, induced mutagenesis, TILLING/EcoTILLING, RNA interference, and precise genome editing with CRISPR/Cas systems are explored as practical tools for reducing susceptibility. Targeted manipulation of eTFs offers a promising avenue to reprogram plants for resistance while maintaining essential cellular functions. By integrating molecular biology with applied strategies, we propose an eTF-centered framework for resistance breeding within a broader stress biology perspective. Future research combining functional genomics, synthetic biology, and breeding innovation will be pivotal in delivering broad-spectrum, durable, and environmentally sustainable resistance to plant viral stress.
{"title":"Molecular gatekeepers: eukaryotic translation factors decoding plant-virus dynamics for resistance engineering.","authors":"Pankhuri Singhal, Shubham Saini, Oshin Saini, Ankit Bishnoi, Rashmi E R, Bharat Raj Meena, Jitender Singh, Kalenahalli Yogendra","doi":"10.1007/s44154-025-00273-2","DOIUrl":"10.1007/s44154-025-00273-2","url":null,"abstract":"<p><p>Plant viruses are among the most significant biotic stressors, posing a severe threat to crop productivity and global food security. Their success largely depends on the exploitation of host eukaryotic translation factors (eTFs), including initiation factors (eIFs) and elongation factors (eEFs), which act as molecular gatekeepers of the viral life cycle. Key members such as eIF4E, eIF(iso)4E, eIF4G, eEF1A, and eEF1B have been identified as susceptibility factors that mediate viral translation, replication, and systemic movement. Viruses have co-evolved specialized proteins and RNA elements, including VPg and IRES structures, to hijack these host factors and circumvent plant defense barriers. This review synthesizes current understanding of the mechanistic roles of eTFs in virus-host dynamics and highlights strategies to mitigate viral stress. Approaches such as natural allele mining, induced mutagenesis, TILLING/EcoTILLING, RNA interference, and precise genome editing with CRISPR/Cas systems are explored as practical tools for reducing susceptibility. Targeted manipulation of eTFs offers a promising avenue to reprogram plants for resistance while maintaining essential cellular functions. By integrating molecular biology with applied strategies, we propose an eTF-centered framework for resistance breeding within a broader stress biology perspective. Future research combining functional genomics, synthetic biology, and breeding innovation will be pivotal in delivering broad-spectrum, durable, and environmentally sustainable resistance to plant viral stress.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"9"},"PeriodicalIF":5.8,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12847506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146055313","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}
Leaf shape plays a crucial role in plant growth and development. Among various leaf traits, marginal lobation serves as an ideal morphological marker for breeding programs. However, the genetic mechanism underlying leaf margin lobation in Brassica juncea L. remains unclear. Through RNA sequencing and map-based cloning, we identified an incompletely dominant gene, BjA10.LL, which encodes an HD-ZIP I protein and is responsible for the formation of leaf margin lobation in B. juncea. Sequence analysis of parental alleles revealed no critical variations in the coding region but identified substantial variations in regulatory regions. Heterologous expression of BjA10.LL in Arabidopsis thaliana confirmed its sufficiency to induce lobed leaves. To functionally link the regulatory variations to the phenotype, we analyzed promoter activity and developed a co-dominant molecular marker targeting key indels in a core enhancer. The promoter activity was significantly affected by these sequence variations, and the marker exhibited perfect co-segregation with the lobed-leaf phenotype in an F₂ population, collectively establishing these regulatory polymorphisms as the causal basis for divergent BjA10.LL expression and leaf morphology. These results demonstrate that BjA10.LL positively regulates marginal lobe formation, providing insights into leaf shape regulation in B. juncea and facilitating the genetic improvement of rapeseed.
{"title":"Cloning and functional analysis of the lobed-leaf gene BjA10.LL in Brassica juncea L.","authors":"Jiajia Liu, Yunyun Ma, Yuxuan He, Xiaohui Cui, Shaojie Ma, Zijin Liu, Saiqi Yang, Yuan Guo, Mingxun Chen","doi":"10.1007/s44154-025-00280-3","DOIUrl":"10.1007/s44154-025-00280-3","url":null,"abstract":"<p><p>Leaf shape plays a crucial role in plant growth and development. Among various leaf traits, marginal lobation serves as an ideal morphological marker for breeding programs. However, the genetic mechanism underlying leaf margin lobation in Brassica juncea L. remains unclear. Through RNA sequencing and map-based cloning, we identified an incompletely dominant gene, BjA10.LL, which encodes an HD-ZIP I protein and is responsible for the formation of leaf margin lobation in B. juncea. Sequence analysis of parental alleles revealed no critical variations in the coding region but identified substantial variations in regulatory regions. Heterologous expression of BjA10.LL in Arabidopsis thaliana confirmed its sufficiency to induce lobed leaves. To functionally link the regulatory variations to the phenotype, we analyzed promoter activity and developed a co-dominant molecular marker targeting key indels in a core enhancer. The promoter activity was significantly affected by these sequence variations, and the marker exhibited perfect co-segregation with the lobed-leaf phenotype in an F₂ population, collectively establishing these regulatory polymorphisms as the causal basis for divergent BjA10.LL expression and leaf morphology. These results demonstrate that BjA10.LL positively regulates marginal lobe formation, providing insights into leaf shape regulation in B. juncea and facilitating the genetic improvement of rapeseed.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"8"},"PeriodicalIF":5.8,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146004833","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}
Advanced genotyping technologies for understanding the genetic intricacies of fungal pathogens have broad applications in crop protection. Here, we introduce a novel genotyping-by-target sequencing (GBTS) chip, a versatile tool designed for comprehensive genetic analysis of fungal populations. This technology overcomes key limitations of traditional molecular marker-based approaches by providing a more efficient, economic, and streamlined solution while bypassing the need for labor-intensive pathogen culturing. We demonstrate its utility by applying it to profile Puccinia striiformis f. sp. tritici (Pst), the causal agent of wheat stripe rust. Our analysis involved 225 infected leaves collected from wheat fields in the northwest oversummering region for Pst in China. We delineated three genetic groups and revealed frequent gene flow, with closer connectivity between Qinghai and Gansu than either province with Ningxia, a pattern consistent with wind trajectory models. These findings illustrate a highly connected regional epidemic system and highlight the value of the GBTS chip for genomic epidemiology. The methodology established here provides a scalable framework for population genetic studies in other fungal pathogens, promising to enhance disease monitoring and management across agricultural systems.
{"title":"The development and validation of a genotyping-by-target sequencing chip for fungal population genetic analysis.","authors":"Haohao Yan, Zhe Ma, Qiang Yao, Shiqin Cao, Qiuzhen Jia, Jiaqi Li, Jie Zhao, Weiyi Yan, Juhong Ma, Wen Chen, Bo Zhang, Xuezhen Ma, Xiaojie Wang, Dejun Han, Zhensheng Kang, Lili Huang, Qingdong Zeng","doi":"10.1007/s44154-025-00281-2","DOIUrl":"10.1007/s44154-025-00281-2","url":null,"abstract":"<p><p>Advanced genotyping technologies for understanding the genetic intricacies of fungal pathogens have broad applications in crop protection. Here, we introduce a novel genotyping-by-target sequencing (GBTS) chip, a versatile tool designed for comprehensive genetic analysis of fungal populations. This technology overcomes key limitations of traditional molecular marker-based approaches by providing a more efficient, economic, and streamlined solution while bypassing the need for labor-intensive pathogen culturing. We demonstrate its utility by applying it to profile Puccinia striiformis f. sp. tritici (Pst), the causal agent of wheat stripe rust. Our analysis involved 225 infected leaves collected from wheat fields in the northwest oversummering region for Pst in China. We delineated three genetic groups and revealed frequent gene flow, with closer connectivity between Qinghai and Gansu than either province with Ningxia, a pattern consistent with wind trajectory models. These findings illustrate a highly connected regional epidemic system and highlight the value of the GBTS chip for genomic epidemiology. The methodology established here provides a scalable framework for population genetic studies in other fungal pathogens, promising to enhance disease monitoring and management across agricultural systems.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"7"},"PeriodicalIF":5.8,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12812796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145999909","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 : 2026-01-12DOI: 10.1007/s44154-025-00274-1
Halima Jafari, Belete Kuraz Abebe, Li Cong, Zulfiqar Ahmed, Wang Zhaofei, Minhao Sun, Gemingguli Muhatai, Lei Chuzhao, Ruihua Dang
The domestication and selective breeding of horses have profoundly influenced the emergence of adaptive traits and stress resistance mechanisms, shaping modern equine populations. This comprehensive review examines the genomic foundations of these traits, emphasizing recent advancements in high-throughput sequencing technologies and bioinformatics. These tools have elucidated the genetic underpinnings of key characteristics such as endurance, speed, metabolic efficiency, and disease resistance. Importantly, the review identifies and connects gene variants associated with thermoregulation, immune function, and cellular repair mechanisms, shedding light on their synergistic roles in enabling horses to adapt to diverse environmental challenges and physiological stressors. By establishing these causal links, this review enhances the coherence between genomic findings and their implications for equine biology. Furthermore, the integration of genomic insights provides a framework for addressing contemporary challenges in horse management and conservation. Issues such as climate change, disease outbreaks, and the preservation of genetic diversity demand innovative strategies grounded in genomics. By bridging the findings on equine adaptation and stress resistance mechanisms with practical applications in breeding and management, this review highlights the potential of genomics to ensure the sustainability and resilience of equine populations in the face of evolving environmental and societal pressures. This expanded perspective underscores the critical role of genomics in both understanding the evolutionary trajectory of horses and guiding future practices in equine health and conservation.
{"title":"Review: Genomic insights into the adaptive traits and stress resistance in modern horses.","authors":"Halima Jafari, Belete Kuraz Abebe, Li Cong, Zulfiqar Ahmed, Wang Zhaofei, Minhao Sun, Gemingguli Muhatai, Lei Chuzhao, Ruihua Dang","doi":"10.1007/s44154-025-00274-1","DOIUrl":"10.1007/s44154-025-00274-1","url":null,"abstract":"<p><p>The domestication and selective breeding of horses have profoundly influenced the emergence of adaptive traits and stress resistance mechanisms, shaping modern equine populations. This comprehensive review examines the genomic foundations of these traits, emphasizing recent advancements in high-throughput sequencing technologies and bioinformatics. These tools have elucidated the genetic underpinnings of key characteristics such as endurance, speed, metabolic efficiency, and disease resistance. Importantly, the review identifies and connects gene variants associated with thermoregulation, immune function, and cellular repair mechanisms, shedding light on their synergistic roles in enabling horses to adapt to diverse environmental challenges and physiological stressors. By establishing these causal links, this review enhances the coherence between genomic findings and their implications for equine biology. Furthermore, the integration of genomic insights provides a framework for addressing contemporary challenges in horse management and conservation. Issues such as climate change, disease outbreaks, and the preservation of genetic diversity demand innovative strategies grounded in genomics. By bridging the findings on equine adaptation and stress resistance mechanisms with practical applications in breeding and management, this review highlights the potential of genomics to ensure the sustainability and resilience of equine populations in the face of evolving environmental and societal pressures. This expanded perspective underscores the critical role of genomics in both understanding the evolutionary trajectory of horses and guiding future practices in equine health and conservation.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"5"},"PeriodicalIF":5.8,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12791104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954037","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}
Cryptocaryon irritans is an obligate parasitic ciliate that significantly endangers marine fish. Hypoxia suppresses the development and hatchability of C. irritans during the tomont stage, which often develops on the seafloor under hypoxic conditions. Despite this knowledge, the underlying adaptation mechanisms of tomonts remain poorly understood. We aimed to determine how hypoxia reprograms tomont metabolism and whether ferroptosis contributes to hypoxia-induced vulnerability. Herein, metabolomic profiling revealed 2,964 differential metabolites under hypoxia. Notably, there were significantly elevated glucose levels, suggesting enhanced glycolytic activity. Enzymatic and qRT-PCR analyses further confirmed hypoxia-induced metabolic reprogramming, including increased hexokinase and pyruvate kinase activities and upregulation of glycolysis-related genes. Hypoxia also induced surface depressions, disrupted cell walls, mitochondrial deformation, reduced mitochondrial membrane potential, disrupted energy homeostasis, and increased NAD⁺/NADH ratio fluctuations and lactate accumulation. To probe ferroptotic susceptibility under hypoxia, hypoxic tomonts were exposed to the ferroptosis inducer erastin, resulting in a hatchability of 13% and promoting reactive oxygen species (ROS) accumulation, lipid peroxidation, and mitochondrial damage. Fluorescence staining revealed strong PI and ROS signals in hypoxic tomonts exposed to the ferroptosis inducer erastin. Notably, mitochondrial dysfunction was accompanied by Ca2⁺ and Fe2⁺ accumulation. Ferroptosis-related genes were upregulated at 24 h post-hypoxia induction. In contrast, gpx4 and mitochondrial electron transport chain components were downregulated at 48 h post-hypoxia induction. These findings demonstrate that hypoxia triggers glycolytic reprogramming and mitochondrial dysfunction in C. irritans, whereas erastin induces ferroptosis under hypoxic stress. This study provides new insights into protozoan hypoxia adaptation and highlights ferroptosis as a potential therapeutic target for controlling parasitic infections in marine aquaculture.
{"title":"Hypoxia-induced oxidative stress and mitochondrial damage initiate ferroptosis in Cryptocaryon irritans, a protozoan parasite of marine fish.","authors":"Baotun Wang, Zhi Luo, Jingyu Zhuang, Zhicheng Li, Xueli Lai, Huicheng Wu, Qing Han, Jizhen Cao, Hebing Wang, Chuanfu Dong, Anxing Li","doi":"10.1007/s44154-025-00275-0","DOIUrl":"10.1007/s44154-025-00275-0","url":null,"abstract":"<p><p>Cryptocaryon irritans is an obligate parasitic ciliate that significantly endangers marine fish. Hypoxia suppresses the development and hatchability of C. irritans during the tomont stage, which often develops on the seafloor under hypoxic conditions. Despite this knowledge, the underlying adaptation mechanisms of tomonts remain poorly understood. We aimed to determine how hypoxia reprograms tomont metabolism and whether ferroptosis contributes to hypoxia-induced vulnerability. Herein, metabolomic profiling revealed 2,964 differential metabolites under hypoxia. Notably, there were significantly elevated glucose levels, suggesting enhanced glycolytic activity. Enzymatic and qRT-PCR analyses further confirmed hypoxia-induced metabolic reprogramming, including increased hexokinase and pyruvate kinase activities and upregulation of glycolysis-related genes. Hypoxia also induced surface depressions, disrupted cell walls, mitochondrial deformation, reduced mitochondrial membrane potential, disrupted energy homeostasis, and increased NAD⁺/NADH ratio fluctuations and lactate accumulation. To probe ferroptotic susceptibility under hypoxia, hypoxic tomonts were exposed to the ferroptosis inducer erastin, resulting in a hatchability of 13% and promoting reactive oxygen species (ROS) accumulation, lipid peroxidation, and mitochondrial damage. Fluorescence staining revealed strong PI and ROS signals in hypoxic tomonts exposed to the ferroptosis inducer erastin. Notably, mitochondrial dysfunction was accompanied by Ca<sup>2</sup>⁺ and Fe<sup>2</sup>⁺ accumulation. Ferroptosis-related genes were upregulated at 24 h post-hypoxia induction. In contrast, gpx4 and mitochondrial electron transport chain components were downregulated at 48 h post-hypoxia induction. These findings demonstrate that hypoxia triggers glycolytic reprogramming and mitochondrial dysfunction in C. irritans, whereas erastin induces ferroptosis under hypoxic stress. This study provides new insights into protozoan hypoxia adaptation and highlights ferroptosis as a potential therapeutic target for controlling parasitic infections in marine aquaculture.</p>","PeriodicalId":74874,"journal":{"name":"Stress biology","volume":"6 1","pages":"6"},"PeriodicalIF":5.8,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12791103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954058","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}