Intestinal telocytes that reside immediately beneath the intestinal epithelium exert niche-supporting roles for intestinal stem cells and their progenies. They are heterogeneous cells compartmentalized along the crypt-villus axis, but the mechanisms governing the maintenance of this telocyte population remain unclear. Here, we identify a distinct population of subepithelial mesenchymal cells in the developing mouse embryo, marked by LIM Domain Only 3 (Lmo3), as the cellular origin of post-natal intestinal telocytes. The Lmo3+ cells emerge prior to villus formation at embryonic day 13.5, and after birth, they progressively acquire a spatial confinement to the intestinal isthmus region, where they persist as long-lived, slow-cycling cells, supplying both peri-villus and peri-crypt telocytes. Further, we show that Lmo3+ cells respond rapidly to tissue damage, becoming activated to promote repair of the telocyte niche. Therefore, a quiescent and damage-responsive progenitor cell population marked by Lmo3 maintains the intestinal telocyte niche.
{"title":"Lmo3-expressing peri-isthmus progenitor cells sustain renewal and repair of the mammalian intestinal telocyte niche","authors":"Daxin Jiang, Guoli Zhu, Yongchao Zhang, Jiawen Wang, Nannan Qian, Zhen Jin, Qingyu Sun, Haimeng Yu, Kebei Tang, Tao Cai, Fengchao Wang, Rongwen Xi","doi":"10.1016/j.devcel.2025.09.004","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.09.004","url":null,"abstract":"Intestinal telocytes that reside immediately beneath the intestinal epithelium exert niche-supporting roles for intestinal stem cells and their progenies. They are heterogeneous cells compartmentalized along the crypt-villus axis, but the mechanisms governing the maintenance of this telocyte population remain unclear. Here, we identify a distinct population of subepithelial mesenchymal cells in the developing mouse embryo, marked by <em>LIM Domain Only 3</em> (<em>Lmo3</em>), as the cellular origin of post-natal intestinal telocytes. The <em>Lmo3</em><sup><em>+</em></sup> cells emerge prior to villus formation at embryonic day 13.5, and after birth, they progressively acquire a spatial confinement to the intestinal isthmus region, where they persist as long-lived, slow-cycling cells, supplying both peri-villus and peri-crypt telocytes. Further, we show that <em>Lmo3</em><sup>+</sup> cells respond rapidly to tissue damage, becoming activated to promote repair of the telocyte niche. Therefore, a quiescent and damage-responsive progenitor cell population marked by <em>Lmo3</em> maintains the intestinal telocyte niche.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"94 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145141185","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 : 2025-09-25DOI: 10.1016/j.devcel.2025.09.003
Zhangmeng Du, Zeyuan Guan, Hai Liu, Jie Zhang, Haitao He, Zhiwen Zheng, Wenhui Zhang, Lihuan Jiang, Jiaqi Zuo, Yan Liu, Beijing Wan, Haifu Tu, Faming Dong, Xuelei Lai, Lizhong Xiong, Ping Yin, Shaowu Xue, Yanke Chen, Zhu Liu
Phosphorus is an essential macronutrient for plants, primarily absorbed from the soil as inorganic phosphate (Pi) through root-located Pi transporters. Despite decades of research into these transporters as targets for developing Pi-efficient crops, their mechanisms for Pi import remain poorly understood. Here, we present the cryo-electron microscopy (cryo-EM) structures of the rice Pi importer OsPHT1;11 in both Pi-bound and unbound forms, characterize its conformational dynamics, and demonstrate how these dynamics contribute to its transport function. Pi is recognized through conserved residues found in plants, with its translocation facilitated by a typical alternating-access mechanism. Single-molecule fluorescence resonance energy transfer (smFRET) analyses show that this transporter undergoes dynamic conformational fluctuations, which are differentially linked to its Pi transport capability, with a predominance of extracellular open conformations favoring Pi transport, while more populated intracellular open conformations hinder it. These findings highlight key conformational determinants of transport activity and provide mechanistic insights into Pi uptake in plants.
{"title":"Cryo-EM structure and dynamic basis of phosphate uptake by PHT1 in rice","authors":"Zhangmeng Du, Zeyuan Guan, Hai Liu, Jie Zhang, Haitao He, Zhiwen Zheng, Wenhui Zhang, Lihuan Jiang, Jiaqi Zuo, Yan Liu, Beijing Wan, Haifu Tu, Faming Dong, Xuelei Lai, Lizhong Xiong, Ping Yin, Shaowu Xue, Yanke Chen, Zhu Liu","doi":"10.1016/j.devcel.2025.09.003","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.09.003","url":null,"abstract":"Phosphorus is an essential macronutrient for plants, primarily absorbed from the soil as inorganic phosphate (Pi) through root-located Pi transporters. Despite decades of research into these transporters as targets for developing Pi-efficient crops, their mechanisms for Pi import remain poorly understood. Here, we present the cryo-electron microscopy (cryo-EM) structures of the rice Pi importer OsPHT1;11 in both Pi-bound and unbound forms, characterize its conformational dynamics, and demonstrate how these dynamics contribute to its transport function. Pi is recognized through conserved residues found in plants, with its translocation facilitated by a typical alternating-access mechanism. Single-molecule fluorescence resonance energy transfer (smFRET) analyses show that this transporter undergoes dynamic conformational fluctuations, which are differentially linked to its Pi transport capability, with a predominance of extracellular open conformations favoring Pi transport, while more populated intracellular open conformations hinder it. These findings highlight key conformational determinants of transport activity and provide mechanistic insights into Pi uptake in plants.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"193 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140955","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 : 2025-09-24DOI: 10.1016/j.devcel.2025.08.017
Catherine A. Tower, Gabriel Manske, Emily L. Ferrell, Dilara N. Anbarci, Kelsey Jorgensen, Binbin Ma, Mansour Aboelenain, Rajesh Ranjan, Saikat Chakraborty, Lindsay Moritz, Arunika Das, Michele Boiani, Ben E. Black, Shawn Chavez, Erica E. Marsh, Ariella Shikanov, Karen Schindler, Xin Chen, Saher Sue Hammoud
Across metazoan species, the centromere-specific histone variant CENP-A is essential for accurate chromosome segregation, yet its regulation during the mammalian parental-to-zygote transition is poorly understood. To address this, we generated a CENP-A-mScarlet mouse model that revealed sex-specific dynamics: mature sperm retain 10% of the CENP-A levels present in MII oocytes. However, this difference is resolved in zygotes prior to the first mitosis, using maternally inherited cytoplasmic CENP-A. Notably, the increase in CENP-A at paternal centromeres is independent of sensing CENP-A asymmetry or the presence of maternal chromosomes. Instead, CENP-A equalization relies on the asymmetric recruitment of maternal CENP-C to paternal centromeres. Depletion of maternal CENP-A decreases total CENP-A in both pronuclei without disrupting equalization. In contrast, reducing maternal CENP-C or disruption of its dimerization function impairs CENP-A equalization and chromosome segregation. Therefore, maternal CENP-C acts as a key epigenetic regulator that resets centromeric symmetry at fertilization to preserve genome integrity.
{"title":"Maternal CENP-C restores centromere symmetry in mammalian zygotes to ensure proper chromosome segregation","authors":"Catherine A. Tower, Gabriel Manske, Emily L. Ferrell, Dilara N. Anbarci, Kelsey Jorgensen, Binbin Ma, Mansour Aboelenain, Rajesh Ranjan, Saikat Chakraborty, Lindsay Moritz, Arunika Das, Michele Boiani, Ben E. Black, Shawn Chavez, Erica E. Marsh, Ariella Shikanov, Karen Schindler, Xin Chen, Saher Sue Hammoud","doi":"10.1016/j.devcel.2025.08.017","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.017","url":null,"abstract":"Across metazoan species, the centromere-specific histone variant CENP-A is essential for accurate chromosome segregation, yet its regulation during the mammalian parental-to-zygote transition is poorly understood. To address this, we generated a CENP-A-mScarlet mouse model that revealed sex-specific dynamics: mature sperm retain 10% of the CENP-A levels present in MII oocytes. However, this difference is resolved in zygotes prior to the first mitosis, using maternally inherited cytoplasmic CENP-A. Notably, the increase in CENP-A at paternal centromeres is independent of sensing CENP-A asymmetry or the presence of maternal chromosomes. Instead, CENP-A equalization relies on the asymmetric recruitment of maternal CENP-C to paternal centromeres. Depletion of maternal CENP-A decreases total CENP-A in both pronuclei without disrupting equalization. In contrast, reducing maternal CENP-C or disruption of its dimerization function impairs CENP-A equalization and chromosome segregation. Therefore, maternal CENP-C acts as a key epigenetic regulator that resets centromeric symmetry at fertilization to preserve genome integrity.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"11 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127337","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.2025.07.012
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}
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