Pub Date : 2025-09-22DOI: 10.1016/j.devcel.2025.07.012
Yan Xiong, Per-Olof Berggren
In this issue of Developmental Cell, Jun, Nguyen-Ngoc et al. report that embedding human pluripotent stem cell-derived islets with endothelial cells and fibroblasts, which form perfusable microvessels, accelerates β cell functional maturation. Endothelial cell-derived extracellular matrix proteins and BMP2/4 enhance the β cell Ca2⁺ response, insulin secretion, and in vivo graft performance.
{"title":"Vascularizing stem cell-derived islets: A blueprint for functional maturation","authors":"Yan Xiong, Per-Olof Berggren","doi":"10.1016/j.devcel.2025.07.012","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.07.012","url":null,"abstract":"In this issue of <em>Developmental Cell</em>, Jun, Nguyen-Ngoc et al. report that embedding human pluripotent stem cell-derived islets with endothelial cells and fibroblasts, which form perfusable microvessels, accelerates β cell functional maturation. Endothelial cell-derived extracellular matrix proteins and BMP2/4 enhance the β cell Ca<sup>2</sup>⁺ response, insulin secretion, and <em>in vivo</em> graft performance.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"21 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-22DOI: 10.1016/j.devcel.2025.06.039
Emily R. Wilson, Xiaoyang Zhang
Precise spatial and temporal control of gene expression, orchestrated by cis-regulatory elements, is essential for diverse cell-type specification during mammalian development. In this issue of Developmental Cell, Amblard et al. dissect the cis-regulatory logic governing Cdx2 expression during caudal body development, identifying a dynamic regulatory code fine-tuning gene expression.
{"title":"Enhancers, silencers, and attenuators: A dynamic and reversible regulatory code","authors":"Emily R. Wilson, Xiaoyang Zhang","doi":"10.1016/j.devcel.2025.06.039","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.06.039","url":null,"abstract":"Precise spatial and temporal control of gene expression, orchestrated by <em>cis</em>-regulatory elements, is essential for diverse cell-type specification during mammalian development. In this issue of <em>Developmental Cell</em>, Amblard et al. dissect the <em>cis</em>-regulatory logic governing <em>Cdx2</em> expression during caudal body development, identifying a dynamic regulatory code fine-tuning gene expression.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"16 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-22DOI: 10.1016/j.devcel.2025.07.002
Xintong Zhang, Yaru Du, Axel Behrens, Linxiang Lan
Lineage plasticity, the ability of cells to switch from one specialized identity to another, is a fundamental cellular process in embryonic development and tissue regeneration. The process is often hijacked by tumor cells at various stages to facilitate cancer initiation, progression, metastasis, and therapy resistance. It is also recognized as a key contributor to intratumor heterogeneity (ITH). In pancreatic ductal adenocarcinoma (PDAC), lineage plasticity is central to acinar-to-ductal metaplasia (ADM) and its associated acinar-to-ductal reprogramming (ADR), epithelial-mesenchymal transition (EMT), cancer stem cell (CSC) regeneration, and molecular subtype rewiring. These mechanisms generate diverse lineage trajectories that shape PDAC development, progression, and therapeutic outcomes. In this review, we discuss how normal and tumor cells in the pancreatic epithelium acquire lineage plasticity and its implications for PDAC pathogenesis, ITH, metastasis, and therapy resistance. We also highlight recent discoveries suggesting potential therapeutic strategies targeting key regulators of lineage plasticity in PDAC.
{"title":"Emerging insights into lineage plasticity in pancreatic cancer initiation, progression, and therapy resistance","authors":"Xintong Zhang, Yaru Du, Axel Behrens, Linxiang Lan","doi":"10.1016/j.devcel.2025.07.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.07.002","url":null,"abstract":"Lineage plasticity, the ability of cells to switch from one specialized identity to another, is a fundamental cellular process in embryonic development and tissue regeneration. The process is often hijacked by tumor cells at various stages to facilitate cancer initiation, progression, metastasis, and therapy resistance. It is also recognized as a key contributor to intratumor heterogeneity (ITH). In pancreatic ductal adenocarcinoma (PDAC), lineage plasticity is central to acinar-to-ductal metaplasia (ADM) and its associated acinar-to-ductal reprogramming (ADR), epithelial-mesenchymal transition (EMT), cancer stem cell (CSC) regeneration, and molecular subtype rewiring. These mechanisms generate diverse lineage trajectories that shape PDAC development, progression, and therapeutic outcomes. In this review, we discuss how normal and tumor cells in the pancreatic epithelium acquire lineage plasticity and its implications for PDAC pathogenesis, ITH, metastasis, and therapy resistance. We also highlight recent discoveries suggesting potential therapeutic strategies targeting key regulators of lineage plasticity in PDAC.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"14 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-22DOI: 10.1016/j.devcel.2025.08.002
Upendra K. Soni, Q. Richard Lu
Glioblastoma invasion has been linked to mesenchymal states. However, in this issue of Developmental Cell, Wu et al. identify peritumoral, uncommitted oligodendrocyte progenitor-like cells as key invasive drivers that hijack neurodevelopmental programs to infiltrate the brain parenchyma, suggesting that targeting lineage differentiation and neuron-tumor networks may limit glioblastoma spread.
{"title":"Living on the edge: Uncommitted OPC-like cells drive glioblastoma invasiveness","authors":"Upendra K. Soni, Q. Richard Lu","doi":"10.1016/j.devcel.2025.08.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.002","url":null,"abstract":"Glioblastoma invasion has been linked to mesenchymal states. However, in this issue of <em>Developmental Cell</em>, Wu et al. identify peritumoral, uncommitted oligodendrocyte progenitor-like cells as key invasive drivers that hijack neurodevelopmental programs to infiltrate the brain parenchyma, suggesting that targeting lineage differentiation and neuron-tumor networks may limit glioblastoma spread.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"8 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-18DOI: 10.1016/j.devcel.2025.08.016
Sophie Herszterg, Simone Cicolini, Marc de Gennes, Anqi Huang, Alexis Matamoro-Vidal, Cyrille Alexandre, Matthew Smith, Helena Araujo, Romain Levayer, Jean-Paul Vincent, Guillaume Salbreux
How cell fate decisions and tissue remodeling are coordinated to establish precise and robust patterns is a fundamental question in developmental biology. Here, we investigate this interplay during the refinement of Drosophila wing veins. We show by live imaging that vein refinement is driven initially by local tissue deformation, followed by cell fate adjustments orchestrated by a signaling network involving Notch, EGFR, and Dpp. Dynamic tracking of signaling reporter activity uncovers a wave of Notch signaling that converts wide crude proveins into thin stereotypical veins. Perturbing large-scale convergence and extension does not affect vein refinement, and optogenetically induced veins refine irrespective of their orientation, demonstrating that the signaling network suffices for refinement, independently of large-scale tissue flows. A minimal biophysical description recapitulates the signaling network’s ability to coordinate vein refinement in various experimental situations. Our results illustrate how cell fate decisions are updated for robust patterning in a remodeling tissue.
{"title":"Signaling-dependent refinement of cell fate choice during tissue remodeling in Drosophila pupal wings","authors":"Sophie Herszterg, Simone Cicolini, Marc de Gennes, Anqi Huang, Alexis Matamoro-Vidal, Cyrille Alexandre, Matthew Smith, Helena Araujo, Romain Levayer, Jean-Paul Vincent, Guillaume Salbreux","doi":"10.1016/j.devcel.2025.08.016","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.016","url":null,"abstract":"How cell fate decisions and tissue remodeling are coordinated to establish precise and robust patterns is a fundamental question in developmental biology. Here, we investigate this interplay during the refinement of <em>Drosophila</em> wing veins. We show by live imaging that vein refinement is driven initially by local tissue deformation, followed by cell fate adjustments orchestrated by a signaling network involving Notch, EGFR, and Dpp. Dynamic tracking of signaling reporter activity uncovers a wave of Notch signaling that converts wide crude proveins into thin stereotypical veins. Perturbing large-scale convergence and extension does not affect vein refinement, and optogenetically induced veins refine irrespective of their orientation, demonstrating that the signaling network suffices for refinement, independently of large-scale tissue flows. A minimal biophysical description recapitulates the signaling network’s ability to coordinate vein refinement in various experimental situations. Our results illustrate how cell fate decisions are updated for robust patterning in a remodeling tissue.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"16 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145078552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-16DOI: 10.1016/j.devcel.2025.08.015
Yuqing Ying, Yuanyi Zhou Xiong, Xue Pan, Qiushi Zhang, Jiajia Chen, Yun Zhao, Xue Cai, Xiao Yi, Yi Zhu, Tiannan Guo, Kai Lei
Identifying regulators for tissue regeneration is fundamental for regenerative biology. While transcription dynamics control planarian regeneration initiation, how protein machinery controls regeneration remains unclear, as transcript levels often fail to predict protein abundance. To address this gap, we performed mass-spectrometry-based proteomic analyses of the planarian Schmidtea mediterranea, establishing a spectral library covering ∼10,000 proteins, and employed quantitative approaches to measure proteome dynamics during regeneration. Our study identified upregulated ribosomal proteins, which were supported by ribosome profiling sequencing (Ribo-seq). Combining RNA sequencing (RNA-seq) and Ribo-seq analyses categorized the increased protein abundance into regulatory modes at transcriptional, translational, and protein stability levels. Functional examination identified 25 proteins essential for planarian regeneration. Troponin T was identified as a regulator of regeneration initiation, showing increased protein abundance before upregulation at transcriptional and translational levels, suggesting a regulation of protein stability. In summary, our study demonstrates previously unexplored ribosome-mediated and transcription-independent protein machinery essential for planarian regeneration initiation.
{"title":"Proteomics-based multi-omics identifies the roadmap of transcription-translation-protein dynamics in planarian regeneration","authors":"Yuqing Ying, Yuanyi Zhou Xiong, Xue Pan, Qiushi Zhang, Jiajia Chen, Yun Zhao, Xue Cai, Xiao Yi, Yi Zhu, Tiannan Guo, Kai Lei","doi":"10.1016/j.devcel.2025.08.015","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.015","url":null,"abstract":"Identifying regulators for tissue regeneration is fundamental for regenerative biology. While transcription dynamics control planarian regeneration initiation, how protein machinery controls regeneration remains unclear, as transcript levels often fail to predict protein abundance. To address this gap, we performed mass-spectrometry-based proteomic analyses of the planarian <em>Schmidtea mediterranea</em>, establishing a spectral library covering ∼10,000 proteins, and employed quantitative approaches to measure proteome dynamics during regeneration. Our study identified upregulated ribosomal proteins, which were supported by ribosome profiling sequencing (Ribo-seq). Combining RNA sequencing (RNA-seq) and Ribo-seq analyses categorized the increased protein abundance into regulatory modes at transcriptional, translational, and protein stability levels. Functional examination identified 25 proteins essential for planarian regeneration. Troponin T was identified as a regulator of regeneration initiation, showing increased protein abundance before upregulation at transcriptional and translational levels, suggesting a regulation of protein stability. In summary, our study demonstrates previously unexplored ribosome-mediated and transcription-independent protein machinery essential for planarian regeneration initiation.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"72 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145067881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-11DOI: 10.1016/j.devcel.2025.08.013
Yang Shao, Xunzheng Li, Benhui Shi, Songyang Wang, Zisheng Luo, Yanqun Xu, Baolei Li, Shuqing Feng, Li Liang, Huanquan Zheng, Jiaqi Sun
Autophagosomes originate from and maintain association with the endoplasmic reticulum (ER) during their formation, yet how these processes are molecularly coordinated in plants remains poorly understood. Here, we demonstrate that Arabidopsis autophagy-related protein 18a (ATG18a), a key organizer of early autophagosome formation, undergoes phase separation to form biomolecular condensates on the ER membrane, which progress from highly mobile droplets to stable ring-like structures, while the ER is reshaped. We discovered that ATG18a condensates work together with ROOT HAIR DEFECTIVE3 (RHD3), an ER membrane-shaping protein, with RABC1 serving as a molecular linker between them. Importantly, RABC1 facilitates both RHD3 assembly necessary for the formation of ring-like ER structures and its interaction with ATG18a condensates. These findings reveal a mechanism whereby biomolecular condensates work together with membrane-shaping proteins to reshape specialized membrane domains through wetting interactions, providing an insight into autophagosome formation in plant stress responses.
{"title":"Biomolecular condensates of ATG18 reshape ER for autophagy in plants","authors":"Yang Shao, Xunzheng Li, Benhui Shi, Songyang Wang, Zisheng Luo, Yanqun Xu, Baolei Li, Shuqing Feng, Li Liang, Huanquan Zheng, Jiaqi Sun","doi":"10.1016/j.devcel.2025.08.013","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.013","url":null,"abstract":"Autophagosomes originate from and maintain association with the endoplasmic reticulum (ER) during their formation, yet how these processes are molecularly coordinated in plants remains poorly understood. Here, we demonstrate that <em>Arabidopsis</em> autophagy-related protein 18a (ATG18a), a key organizer of early autophagosome formation, undergoes phase separation to form biomolecular condensates on the ER membrane, which progress from highly mobile droplets to stable ring-like structures, while the ER is reshaped. We discovered that ATG18a condensates work together with ROOT HAIR DEFECTIVE3 (RHD3), an ER membrane-shaping protein, with RABC1 serving as a molecular linker between them. Importantly, RABC1 facilitates both RHD3 assembly necessary for the formation of ring-like ER structures and its interaction with ATG18a condensates. These findings reveal a mechanism whereby biomolecular condensates work together with membrane-shaping proteins to reshape specialized membrane domains through wetting interactions, providing an insight into autophagosome formation in plant stress responses.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"312 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145043287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression. Clinically, elevated O-GlcNAcylated TR11B correlates with advanced LUAD. Genetic deletion of Ogt suppresses tumor development in LUAD mouse models. Importantly, celecoxib, an U.S. Food and Drug Administration (FDA)-approved drug, inhibits O-GlcNAcylation and exerts antitumor effects. These findings reveal a pathological role for cytokine O-GlcNAcylation in LUAD and identify this axis as a potential therapeutic target.
{"title":"A pathological role of O-GlcNAcylation-driven TR11B production and function in lung adenocarcinoma","authors":"Shiyu Qiu, Lifang Ma, Keke Yu, Xin Xu, Xiao Zhang, Wenjun Yu, Kai Wang, Xiaoting Tian, Yayou Miao, Yikun Wang, Wanxin Guo, Xiangfei Xue, Jiangtao Cui, Xuewen Yu, Rui Kang, Qianjun Zhou, Yongchun Yu, Daolin Tang, Jiayi Wang","doi":"10.1016/j.devcel.2025.08.010","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.010","url":null,"abstract":"Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression. Clinically, elevated O-GlcNAcylated TR11B correlates with advanced LUAD. Genetic deletion of <em>Ogt</em> suppresses tumor development in LUAD mouse models. Importantly, celecoxib, an U.S. Food and Drug Administration (FDA)-approved drug, inhibits O-GlcNAcylation and exerts antitumor effects. These findings reveal a pathological role for cytokine O-GlcNAcylation in LUAD and identify this axis as a potential therapeutic target.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"17 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145018073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-08DOI: 10.1016/j.devcel.2025.06.023
Yuan Chen
In this issue of Developmental Cell, Li et al. show that ETS variant transcription factor 1 (Etv1) SUMOylation not only maintains cancer stem cells (CSCs) but also enables their communications with non-CSC cancer cells to induce tumorigenesis of non-CSCs. The finding reveals a new function of CSCs in driving aggressive tumorigenesis that is SUMOylation dependent.
{"title":"SUMOylation of the transcription factor Etv1 in cancer stem cells induces tumorigenesis of non-stem cancer cells","authors":"Yuan Chen","doi":"10.1016/j.devcel.2025.06.023","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.06.023","url":null,"abstract":"In this issue of <em>Developmental Cell</em>, Li et al. show that ETS variant transcription factor 1 (Etv1) SUMOylation not only maintains cancer stem cells (CSCs) but also enables their communications with non-CSC cancer cells to induce tumorigenesis of non-CSCs. The finding reveals a new function of CSCs in driving aggressive tumorigenesis that is SUMOylation dependent.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"7 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145009318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-08DOI: 10.1016/j.devcel.2025.08.008
Ran Lu, Elwira Smakowska-Luzan
In this issue of Developmental Cell, Yuan et al. explores how the pathogenic bacterium Pseudomonas syringae modulates plant metabolism, particularly through methylglyoxal (MG) accumulation, to suppress immune responses in Arabidopsis. By affecting key proteins TTM2 and CAT2, the pathogen reduces hydrogen peroxide levels, weakening plant defense mechanisms and promoting infection.
{"title":"Novel bacterial strategy to hijack plant immunity through metabolic manipulation","authors":"Ran Lu, Elwira Smakowska-Luzan","doi":"10.1016/j.devcel.2025.08.008","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.008","url":null,"abstract":"In this issue of <em>Developmental Cell</em>, Yuan et al. explores how the pathogenic bacterium <em>Pseudomonas syringae</em> modulates plant metabolism, particularly through methylglyoxal (MG) accumulation, to suppress immune responses in <em>Arabidopsis</em>. By affecting key proteins TTM2 and CAT2, the pathogen reduces hydrogen peroxide levels, weakening plant defense mechanisms and promoting infection.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"6 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145009321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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