PIN-mediated auxin transport is crucial for light-regulated plant organogenesis; however, how light modulates PIN localization remains elusive. Cotton (Gossypium hirsutum), a key textile crop, requires ample sunlight for optimal growth and fiber development. Yet, the mechanism underlying light-regulated fiber development is obscure. Our research shows that light promotes fiber initiation and elongation through inhibiting ubiquitylation degradation of GhPIN3a and subsequently enhancing GhPIN3a plasma-membrane localization. In fiber cells, where GhPIN3a undergoes preferential ubiquitylation, GhCOP1 was identified to control ubiquitylation degradation of GhPIN3a in response to light. Dark-stabilized GhCOP1 targets GhUCH3, which interacts with GhPIN3a to balance its stability through deubiquitylation. This regulatory cascade converts light signals into developmental cues in cotton fibers. Intriguingly, while GhCOP1 promotes GhUCH3 degradation via the ubiquitin-proteasome system (UPS), GhUCH3 modulates GhPIN3a proteolysis through both the UPS and the vacuolar degradation pathway. Our findings reveal a light-regulated GhPIN3a stability mechanism through the GhCOP1-GhUCH3 module, consequently influencing cotton fiber development.
{"title":"A light-governed cascade of ubiquitin modifications regulates cotton fiber development by coordinating PIN3a proteolysis.","authors":"Liuqin Zhang,Yanling Zhou,Xingxian Fu,Changzheng Xu,Lina Liu,Xinyue Du,Yahong An,Mingxuan Xu,Liman Mu,Qingqing Li,Jinyu Cui,Lei Hou,Yan Pei,Mi Zhang","doi":"10.1093/plcell/koaf237","DOIUrl":"https://doi.org/10.1093/plcell/koaf237","url":null,"abstract":"PIN-mediated auxin transport is crucial for light-regulated plant organogenesis; however, how light modulates PIN localization remains elusive. Cotton (Gossypium hirsutum), a key textile crop, requires ample sunlight for optimal growth and fiber development. Yet, the mechanism underlying light-regulated fiber development is obscure. Our research shows that light promotes fiber initiation and elongation through inhibiting ubiquitylation degradation of GhPIN3a and subsequently enhancing GhPIN3a plasma-membrane localization. In fiber cells, where GhPIN3a undergoes preferential ubiquitylation, GhCOP1 was identified to control ubiquitylation degradation of GhPIN3a in response to light. Dark-stabilized GhCOP1 targets GhUCH3, which interacts with GhPIN3a to balance its stability through deubiquitylation. This regulatory cascade converts light signals into developmental cues in cotton fibers. Intriguingly, while GhCOP1 promotes GhUCH3 degradation via the ubiquitin-proteasome system (UPS), GhUCH3 modulates GhPIN3a proteolysis through both the UPS and the vacuolar degradation pathway. Our findings reveal a light-regulated GhPIN3a stability mechanism through the GhCOP1-GhUCH3 module, consequently influencing cotton fiber development.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246784","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}
Iron is an essential nutrient for all organisms. Feruloyl-COA 6-hydroxylase 1 (F6'H1) plays a pivotal role in iron uptake in plant roots by catalyzing the biosynthesis of iron-mobilizing scopoletin, a secondary metabolite also possessing antimicrobial activity. However, it remains unclear whether F6'H1-mediated iron uptake affects plant resistance to foliar pathogens and how such a process might be regulated. Here, we show that enhanced expression of 2-oxoglutarate-dependent dioxygenases 2 (CmOGD2), a homolog of F6'H1 in Citron C-05 (Citrus medica L.), confers resistance to citrus canker caused by Xanthomonas citri subsp. citri (Xcc). CmOGD2-mediated pathogen resistance is achieved by promoting iron uptake and the accumulation of reactive oxygen species (ROS), which likely results in ferroptosis. Furthermore, CmOGD2 interacts with the enolase CmENO2 to destabilize CmZAT10.1, a transcriptional activator of CmOGD2, thereby forming a negative feedback loop that limits CmOGD2 expression. Notably, the Xcc effector pthA4 interferes with the CmOGD2-CmENO2 interaction, likely via a decoy mechanism, leading to CmZAT10.1 accumulation. These findings reveal complex regulatory mechanisms underlying the critical role of CmOGD2 in mediating Xcc resistance through iron- and ROS-dependent ferroptosis.
{"title":"Complex regulation of Citron OGD2-dependent resistance to citrus canker caused by Xanthomonas citri subsp. citri.","authors":"Chenxing Hao,Yan Jin,Hanying Su,Jianming Luo,Xuzhao Luo,Mingzhu Yao,Yuting Song,Jian Han,Xiubin Liu,Yu Xu,Yajie Zheng,Zhengmin Yang,Dazhi Li,Xuncheng Liu,Shunyuan Xiao,Xingyao Xiong,Ziniu Deng,Yunlin Cao,Xianfeng Ma","doi":"10.1093/plcell/koaf225","DOIUrl":"https://doi.org/10.1093/plcell/koaf225","url":null,"abstract":"Iron is an essential nutrient for all organisms. Feruloyl-COA 6-hydroxylase 1 (F6'H1) plays a pivotal role in iron uptake in plant roots by catalyzing the biosynthesis of iron-mobilizing scopoletin, a secondary metabolite also possessing antimicrobial activity. However, it remains unclear whether F6'H1-mediated iron uptake affects plant resistance to foliar pathogens and how such a process might be regulated. Here, we show that enhanced expression of 2-oxoglutarate-dependent dioxygenases 2 (CmOGD2), a homolog of F6'H1 in Citron C-05 (Citrus medica L.), confers resistance to citrus canker caused by Xanthomonas citri subsp. citri (Xcc). CmOGD2-mediated pathogen resistance is achieved by promoting iron uptake and the accumulation of reactive oxygen species (ROS), which likely results in ferroptosis. Furthermore, CmOGD2 interacts with the enolase CmENO2 to destabilize CmZAT10.1, a transcriptional activator of CmOGD2, thereby forming a negative feedback loop that limits CmOGD2 expression. Notably, the Xcc effector pthA4 interferes with the CmOGD2-CmENO2 interaction, likely via a decoy mechanism, leading to CmZAT10.1 accumulation. These findings reveal complex regulatory mechanisms underlying the critical role of CmOGD2 in mediating Xcc resistance through iron- and ROS-dependent ferroptosis.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"86 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254761","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}
The rice (Oryza sativa) PSEUDO-ETIOLATION IN LIGHT (OsPEL) microProtein family members function as dominant-negative regulators of chloroplast development and are conserved among land plants. Knockout of all three OsPEL genes enhanced plant greening traits and was accompanied by leaf anatomical modifications associated with chloroplast-enriched bundle sheath cells in rice. These phenotypic changes correlated with increased CO2 assimilation efficiency and yield. OsPEL1 specifically interacts with key positive regulators of photosynthesis, the rice GOLDEN2-LIKE (OsGLK) transcription factors and the PHOTOSYSTEM I ASSEMBLY 2 (OsPSA2) chaperone. OsPEL1 inhibits these regulators by sequestering OsGLK1 and OsPSA2 in the cytoplasm, which prevents their proper localization to the nucleus and chloroplast, respectively. Supported by RNA-seq evidence of transcriptional homeostasis in greening-related genes, we reveal a multilayered regulatory mechanism and identify the OsPEL family as a promising target for crop improvement.
水稻（Oryza sativa） pseudoetiolation IN LIGHT （OsPEL）微蛋白家族成员是叶绿体发育的显性负调控因子，在陆地植物中是保守的。敲除所有三个OsPEL基因增强了水稻植株的绿化性状，并伴随着与叶绿体富集的束鞘细胞相关的叶片解剖改变。这些表型变化与CO2同化效率和产量的增加相关。OsPEL1特异性地与光合作用的关键正调控因子、水稻GOLDEN2-LIKE （OsGLK）转录因子和光系统I组装2 （OsPSA2）伴侣蛋白相互作用。OsPEL1通过在细胞质中隔离OsGLK1和OsPSA2来抑制这些调节因子，从而阻止它们分别正确定位到细胞核和叶绿体。在绿植相关基因转录稳态的RNA-seq证据的支持下，我们揭示了一个多层调控机制，并确定OsPEL家族是作物改良的一个有希望的目标。
{"title":"Editing of rice PSEUDO-ETIOLATION IN LIGHT microProtein genes promotes chloroplast development","authors":"Heebak Choi, Tae Gyu Yi, Yun-Shil Gho, Ki-Hong Jung, Sun-Hwa Ha","doi":"10.1093/plcell/koaf235","DOIUrl":"https://doi.org/10.1093/plcell/koaf235","url":null,"abstract":"The rice (Oryza sativa) PSEUDO-ETIOLATION IN LIGHT (OsPEL) microProtein family members function as dominant-negative regulators of chloroplast development and are conserved among land plants. Knockout of all three OsPEL genes enhanced plant greening traits and was accompanied by leaf anatomical modifications associated with chloroplast-enriched bundle sheath cells in rice. These phenotypic changes correlated with increased CO2 assimilation efficiency and yield. OsPEL1 specifically interacts with key positive regulators of photosynthesis, the rice GOLDEN2-LIKE (OsGLK) transcription factors and the PHOTOSYSTEM I ASSEMBLY 2 (OsPSA2) chaperone. OsPEL1 inhibits these regulators by sequestering OsGLK1 and OsPSA2 in the cytoplasm, which prevents their proper localization to the nucleus and chloroplast, respectively. Supported by RNA-seq evidence of transcriptional homeostasis in greening-related genes, we reveal a multilayered regulatory mechanism and identify the OsPEL family as a promising target for crop improvement.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235326","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}
Plants are vulnerable to photodamage when exposed to light intensities that exceed their photosynthetic capacity. To protect themselves, they activate Non-Photochemical Quenching (NPQ), a set of processes that dissipate excess excitation energy as heat. NPQ has been studied extensively, but the field remains conceptually fragmented and general consensus on the underlying mechanisms has yet to be reached. Interest in NPQ has recently intensified due to studies showing that tuning NPQ regulation can lead to substantial improvements in photosynthetic efficiency and even crop yield increases of up to 30%. In this review, we aim to bring structure to the diverse and sometimes contradictory NPQ literature by framing the discussion around a set of key mechanistic questions. We focus on the fastest component of NPQ, known as qE, which is activated within the first minutes of excess light exposure. Topics addressed include the molecular properties and roles of PsbS and zeaxanthin, potential conformational changes in light-harvesting complexes (LHCs), reorganization of the thylakoid membrane, and the interplay between these different factors. We synthesize the available evidence into a working model in which qE arises largely from a localized conformational switch in a small number of antenna complexes, triggered by PsbS whereas zeaxanthin increases the domain size of the antenna that can be quenched by each of these quenchers.
{"title":"Non-Photochemical Quenching in Plants: Mechanisms and Mysteries.","authors":"Herbert van Amerongen,Roberta Croce","doi":"10.1093/plcell/koaf240","DOIUrl":"https://doi.org/10.1093/plcell/koaf240","url":null,"abstract":"Plants are vulnerable to photodamage when exposed to light intensities that exceed their photosynthetic capacity. To protect themselves, they activate Non-Photochemical Quenching (NPQ), a set of processes that dissipate excess excitation energy as heat. NPQ has been studied extensively, but the field remains conceptually fragmented and general consensus on the underlying mechanisms has yet to be reached. Interest in NPQ has recently intensified due to studies showing that tuning NPQ regulation can lead to substantial improvements in photosynthetic efficiency and even crop yield increases of up to 30%. In this review, we aim to bring structure to the diverse and sometimes contradictory NPQ literature by framing the discussion around a set of key mechanistic questions. We focus on the fastest component of NPQ, known as qE, which is activated within the first minutes of excess light exposure. Topics addressed include the molecular properties and roles of PsbS and zeaxanthin, potential conformational changes in light-harvesting complexes (LHCs), reorganization of the thylakoid membrane, and the interplay between these different factors. We synthesize the available evidence into a working model in which qE arises largely from a localized conformational switch in a small number of antenna complexes, triggered by PsbS whereas zeaxanthin increases the domain size of the antenna that can be quenched by each of these quenchers.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240920","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}
Enhancers control gene expression, orchestrating plant development and responses to stimuli. However, the regulatory codes of enhancers that confer tissue-specific expression in plants remain largely unexplored. Using massively parallel reporter assays (MPRAs) in tomato tissues, we tested the enhancer activity of 11,180 promoter fragments derived from fruit-specific genes. We discovered 2,436 active fruit enhancer sequences, a subset of which showed differential activity between fruit and leaves, suggesting that they can drive fruit-specific gene expression in tomato. We dissected the sequence determinants of fruit enhancers using deep learning. Guided by the regulatory rules learned from our MPRA dataset, we designed synthetic enhancers and experimentally validated their ability to specifically target tomato fruit. Our study provides a comprehensive landscape of functional enhancers in tomato fruit, facilitating the de novo design of synthetic enhancers for tissue-specific gene expression in plants.
{"title":"Decoding tissue-specific enhancers in plants using massively parallel assays and deep learning.","authors":"Yaxin Deng,Weihua Zhao,Yixue Xiong,Muhammad Naeem,Shan Lu,Xuanwei Zhou,Lingxia Zhao,Lida Zhang","doi":"10.1093/plcell/koaf236","DOIUrl":"https://doi.org/10.1093/plcell/koaf236","url":null,"abstract":"Enhancers control gene expression, orchestrating plant development and responses to stimuli. However, the regulatory codes of enhancers that confer tissue-specific expression in plants remain largely unexplored. Using massively parallel reporter assays (MPRAs) in tomato tissues, we tested the enhancer activity of 11,180 promoter fragments derived from fruit-specific genes. We discovered 2,436 active fruit enhancer sequences, a subset of which showed differential activity between fruit and leaves, suggesting that they can drive fruit-specific gene expression in tomato. We dissected the sequence determinants of fruit enhancers using deep learning. Guided by the regulatory rules learned from our MPRA dataset, we designed synthetic enhancers and experimentally validated their ability to specifically target tomato fruit. Our study provides a comprehensive landscape of functional enhancers in tomato fruit, facilitating the de novo design of synthetic enhancers for tissue-specific gene expression in plants.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194724","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}
Cold stress limits the growth, development and yield of maize (Zea mays L.). Mitogen-activated protein kinases (MAPKs) play important roles in response to cold stress. However, besides the canonical MAPK cascades, it is unclear whether other kinases directly activate MAPKs under cold stress. Here, we identified brassinosteroid-signaling kinase 4 (ZmBSK4) as an upstream kinase of ZmMAPK4 in regulating cold tolerance. Functional analysis demonstrated that ZmMAPK4 and ZmBSK4 positively regulate cold tolerance in maize. ZmBSK4 directly interacts with and phosphorylates ZmMAPK4 at Ser-171. This Ser-171 phosphorylation augments ZmMAPK4 kinase activity and improves maize cold tolerance. Furthermore, we identified two ZmMAPK4-interacting substrates: the two basic helix-loop-helix (bHLH) transcription factors ZmbHLH111 and ZmbHLH181. ZmMAPK4 phosphorylates ZmbHLH111 and ZmbHLH181. Ser-171 phosphorylation enhances ZmMAPK4-mediated phosphorylation of ZmbHLH111 and ZmbHLH181, which promotes their transcriptional activity. Then, ZmbHLH111 and ZmbHLH181 induce the expression of the cold-responsive genes Zea mays dehydration response element binding protein1.2/1.4/1.9/1.10 (ZmDREB1.2/1.4/1.9/1.10), thereby enhancing cold tolerance in maize. Taken together, ZmBSK4 phosphorylating ZmMAPK4 at Ser-171 enhances ZmMAPK4-mediated phosphorylation of ZmbHLH111 and ZmbHLH181, which promotes their activity, ultimately triggering the expression of the cold-responsive ZmDREB1 genes and enhancing maize cold tolerance. Our results reveal a non-canonical MAPK regulatory mechanism for enhancing cold tolerance in maize.
{"title":"Brassinosteroid-signaling kinase 4 activates mitogen-activated protein kinase 4 to enhance cold stress tolerance in maize.","authors":"Chen Zhang,Guangdong Li,Yitian Pan,Qian Li,Yadan Miao,Yang Xiang,Aying Zhang","doi":"10.1093/plcell/koaf234","DOIUrl":"https://doi.org/10.1093/plcell/koaf234","url":null,"abstract":"Cold stress limits the growth, development and yield of maize (Zea mays L.). Mitogen-activated protein kinases (MAPKs) play important roles in response to cold stress. However, besides the canonical MAPK cascades, it is unclear whether other kinases directly activate MAPKs under cold stress. Here, we identified brassinosteroid-signaling kinase 4 (ZmBSK4) as an upstream kinase of ZmMAPK4 in regulating cold tolerance. Functional analysis demonstrated that ZmMAPK4 and ZmBSK4 positively regulate cold tolerance in maize. ZmBSK4 directly interacts with and phosphorylates ZmMAPK4 at Ser-171. This Ser-171 phosphorylation augments ZmMAPK4 kinase activity and improves maize cold tolerance. Furthermore, we identified two ZmMAPK4-interacting substrates: the two basic helix-loop-helix (bHLH) transcription factors ZmbHLH111 and ZmbHLH181. ZmMAPK4 phosphorylates ZmbHLH111 and ZmbHLH181. Ser-171 phosphorylation enhances ZmMAPK4-mediated phosphorylation of ZmbHLH111 and ZmbHLH181, which promotes their transcriptional activity. Then, ZmbHLH111 and ZmbHLH181 induce the expression of the cold-responsive genes Zea mays dehydration response element binding protein1.2/1.4/1.9/1.10 (ZmDREB1.2/1.4/1.9/1.10), thereby enhancing cold tolerance in maize. Taken together, ZmBSK4 phosphorylating ZmMAPK4 at Ser-171 enhances ZmMAPK4-mediated phosphorylation of ZmbHLH111 and ZmbHLH181, which promotes their activity, ultimately triggering the expression of the cold-responsive ZmDREB1 genes and enhancing maize cold tolerance. Our results reveal a non-canonical MAPK regulatory mechanism for enhancing cold tolerance in maize.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"102 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194498","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}
S Einspanier, C Tominello-Ramirez, F Delplace, R Stam
Wild relatives of crop species possess diverse levels of quantitative disease resistance (QDR) to biotic stresses. The genomic and regulatory mechanisms underlying these differences are poorly understood. How QDR against a generalist necrotrophic pathogen evolved and whether it is driven by conserved or species-specific regulatory networks remains unclear. We examined the transcriptomic responses of five diverse wild tomato species that span a gradient of QDR. We initially hypothesized that conserved regulatory modules might control QDR. We use differential gene expression analysis and weighted gene co-expression network analysis (WGCNA) to find instead that species-specific regulatory features, encompassing both infection-induced and constitutively expressed genes, predominantly shape QDR levels. To further dissect the evolutionary basis of these regulatory patterns, we performed phylotranscriptomic analyses of gene regulatory networks. Notably, our findings reveal that the conserved NAC transcription factor 29 is pivotal in developing disease resistance only in S. pennellii. The differential regulation and altered downstream signaling pathways of NAC29 provide evidence for its co-option in the resistance mechanisms of S. pennellii. The role of NAC29 in conferring resistance is confirmed by the presence of a premature stop codon in susceptible S. pennellii genotypes. This finding highlights the species-specific rewiring of gene regulatory networks by repurposing a conserved regulatory element to effectively enhance resistance against pathogens. These results offer insights into the evolutionary and regulatory complexity underlying QDR and emphasize the significance of species-specific gene regulation in shaping resistance against a cosmopolitan necrotrophic pathogen.
{"title":"Co-option of transcription factors drives evolution of quantitative disease resistance against a necrotrophic pathogen","authors":"S Einspanier, C Tominello-Ramirez, F Delplace, R Stam","doi":"10.1093/plcell/koaf233","DOIUrl":"https://doi.org/10.1093/plcell/koaf233","url":null,"abstract":"Wild relatives of crop species possess diverse levels of quantitative disease resistance (QDR) to biotic stresses. The genomic and regulatory mechanisms underlying these differences are poorly understood. How QDR against a generalist necrotrophic pathogen evolved and whether it is driven by conserved or species-specific regulatory networks remains unclear. We examined the transcriptomic responses of five diverse wild tomato species that span a gradient of QDR. We initially hypothesized that conserved regulatory modules might control QDR. We use differential gene expression analysis and weighted gene co-expression network analysis (WGCNA) to find instead that species-specific regulatory features, encompassing both infection-induced and constitutively expressed genes, predominantly shape QDR levels. To further dissect the evolutionary basis of these regulatory patterns, we performed phylotranscriptomic analyses of gene regulatory networks. Notably, our findings reveal that the conserved NAC transcription factor 29 is pivotal in developing disease resistance only in S. pennellii. The differential regulation and altered downstream signaling pathways of NAC29 provide evidence for its co-option in the resistance mechanisms of S. pennellii. The role of NAC29 in conferring resistance is confirmed by the presence of a premature stop codon in susceptible S. pennellii genotypes. This finding highlights the species-specific rewiring of gene regulatory networks by repurposing a conserved regulatory element to effectively enhance resistance against pathogens. These results offer insights into the evolutionary and regulatory complexity underlying QDR and emphasize the significance of species-specific gene regulation in shaping resistance against a cosmopolitan necrotrophic pathogen.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145195148","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}
Miaoyuan Hua,Wenzhe Yin,Alison C Tidy,José Fernández Gómez,Huanjun Li,Shuya Shi,Guangwei Xing,Jie Zong,Zoe A Wilson
The production of viable pollen is essential for effective fertilization and optimal crop yields; however, our understanding of the underlying mechanisms remains limited. Here, we characterize a barley (Hordeum vulgare) anther bHLH gene, DEFECTIVE TAPETUM TRANSITION1 (DTT1), a gatekeeper that regulates tapetum development. The dtt1 mutant is male sterile, failing to acquire tapetum cell fate identity with over-proliferation of indeterminate tapetal precursor cells, a lack of tapetum endomitosis, and cell wall degeneration. DTT1 forms heterodimers with DYSFUNCTIONAL TAPETUM1 (HvDYT1) through bHLH and ACT-like(BIF) domains, with the ACT-like(BIF) domain and the IKL motif critical in partner selection. These heterodimers may subsequently interact with each other through the bHLH-ACT-like(BIF) domain to activate expression. Transcriptome analysis confirmed that anther development transition from stage 6 to 7 fails in dtt1. We show that HvTDF1-related pathways are downstream of DTT1 and work in independent and overlapping networks with other conserved tapetum regulators. SELEX-seq analysis indicates that DTT1 can bind to DNA with a chimeric or canonical E-box motif only when it forms a complex with HvDYT1. In vivo dual-luciferase assays confirmed that the DTT1-HvDYT1 complex directly regulates the expression of several stage 7-specific transcription factors, such as HvTDF1, HvEAT1, and the identified GAMYB target genes. Therefore, the paired DTT1-HvDYT1 complex appears crucial in orchestrating the transition of tapetum cell fate by modulating genes involved in diverse biological pathways. This work uncovers detailed relationships in barley tapetum regulation and male fertility.
{"title":"The bHLH transcription factor DTT1 is part of a paired key that unlocks the tapetum transition in barley anther development.","authors":"Miaoyuan Hua,Wenzhe Yin,Alison C Tidy,José Fernández Gómez,Huanjun Li,Shuya Shi,Guangwei Xing,Jie Zong,Zoe A Wilson","doi":"10.1093/plcell/koaf230","DOIUrl":"https://doi.org/10.1093/plcell/koaf230","url":null,"abstract":"The production of viable pollen is essential for effective fertilization and optimal crop yields; however, our understanding of the underlying mechanisms remains limited. Here, we characterize a barley (Hordeum vulgare) anther bHLH gene, DEFECTIVE TAPETUM TRANSITION1 (DTT1), a gatekeeper that regulates tapetum development. The dtt1 mutant is male sterile, failing to acquire tapetum cell fate identity with over-proliferation of indeterminate tapetal precursor cells, a lack of tapetum endomitosis, and cell wall degeneration. DTT1 forms heterodimers with DYSFUNCTIONAL TAPETUM1 (HvDYT1) through bHLH and ACT-like(BIF) domains, with the ACT-like(BIF) domain and the IKL motif critical in partner selection. These heterodimers may subsequently interact with each other through the bHLH-ACT-like(BIF) domain to activate expression. Transcriptome analysis confirmed that anther development transition from stage 6 to 7 fails in dtt1. We show that HvTDF1-related pathways are downstream of DTT1 and work in independent and overlapping networks with other conserved tapetum regulators. SELEX-seq analysis indicates that DTT1 can bind to DNA with a chimeric or canonical E-box motif only when it forms a complex with HvDYT1. In vivo dual-luciferase assays confirmed that the DTT1-HvDYT1 complex directly regulates the expression of several stage 7-specific transcription factors, such as HvTDF1, HvEAT1, and the identified GAMYB target genes. Therefore, the paired DTT1-HvDYT1 complex appears crucial in orchestrating the transition of tapetum cell fate by modulating genes involved in diverse biological pathways. This work uncovers detailed relationships in barley tapetum regulation and male fertility.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194726","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}
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