Developmental cellPub Date : 2025-09-22DOI: 10.1016/j.devcel.2025.08.002
Upendra K. Soni, Q. Richard Lu
{"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}
Developmental cellPub 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
{"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}
Developmental cellPub 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
{"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}
Developmental cellPub 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
{"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}
Developmental cellPub Date : 2025-09-10DOI: 10.1016/j.devcel.2025.08.012
Philippe Petry, Alexander Oschwald, Simon Merkt, Thien-Ly Julia Dinh, Geoffroy Andrieux, Cylia Crisand, Hannah Botterer, Elisa Nent, Neil Paterson, Monique Havermans, Roman Sankowski, Oliver Schilling, Melanie Boerries, Lukas Amann, Olaf Groß, Andreas Schlitzer, Marco Prinz, Tim Lämmermann, Katrin Kierdorf
{"title":"Early microglia progenitors colonize the embryonic CNS via integrin-mediated migration from the pial surface.","authors":"Philippe Petry, Alexander Oschwald, Simon Merkt, Thien-Ly Julia Dinh, Geoffroy Andrieux, Cylia Crisand, Hannah Botterer, Elisa Nent, Neil Paterson, Monique Havermans, Roman Sankowski, Oliver Schilling, Melanie Boerries, Lukas Amann, Olaf Groß, Andreas Schlitzer, Marco Prinz, Tim Lämmermann, Katrin Kierdorf","doi":"10.1016/j.devcel.2025.08.012","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.012","url":null,"abstract":"<p><p>Macrophage progenitors colonize their anatomical niches in the central nervous system (CNS) in distinct pre- and postnatal waves. Microglia progenitors originate from early erythromyeloid progenitors in the yolk sac and enter the murine CNS around embryonic day (E)9.5. While their developmental origin is well established, the molecular mechanisms guiding CNS colonization are not yet resolved. Using transcriptomic and proteomic approaches, we identified potential factors involved in this process. Microglia progenitors showed a distinct integrin surface profile and transmigrate along the extracellular matrix (ECM)-enriched pial surface into the CNS, pointing to a mesenchyme-to-CNS migration route. Loss of the integrin adaptor protein talin-1 in microglia progenitors led to a reduced CNS colonization, whereas macrophage progenitors in the surrounding mesenchyme remained unchanged. Overall, our data suggest that microglial progenitors enter the CNS parenchyma via talin-1-mediated migration from the surrounding mesenchyme through the ECM-enriched pial surface.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039301","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}
{"title":"Environmental and genetic risk factors of depression converge on neuronal dysfunction driven by changes in cholesterol homeostasis.","authors":"Polina Oberst, Nan Xu, Hermany Munguba, Chao Zhang, Aaron Zhong, Ting Zhou, Conor Liston, Joshua Levitz, Lorenz Studer","doi":"10.1016/j.devcel.2025.08.011","DOIUrl":"10.1016/j.devcel.2025.08.011","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is a complex, multifactorial neuropsychiatric disorder influenced by both genetic and environmental factors, but how these factors impact human neuronal function remains unclear. Using a highly defined human pluripotent stem cell (hPSC)-based prefrontal cortex (PFC) platform, we examined three high-confidence environmental and genetic factors associated with depression: chronic exposure to high levels of cortisol or interferon alpha (IFN-a), and a mutation in SIRTUIN 1 (SIRT1). All three conditions induced overlapping phenotypes of neuronal dysfunction, characterized by dendritic atrophy, synaptic loss, and neuronal hypoactivity across multiple cell lines. RNA sequencing uncovered converging alterations in neuronal cholesterol homeostasis. Depleting cholesterol in control neurons reproduced core depression-associated neuronal phenotypes, while cholesterol supplementation was sufficient to rescue these phenotypes in depression-associated conditions. These findings point to cholesterol imbalance as a common driver of neuronal dysfunction in MDD, linking diverse genetic and environmental risk factors through a shared cellular pathway.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039281","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}
Developmental cellPub Date : 2025-09-09DOI: 10.1016/j.devcel.2025.08.009
Oliver C K Inge, Elias Copin, Jake Cornwall-Scoones, Borzo Gharibi, Irene Rodriguez-Hernandez, Pablo Soro-Barrio, Molly Strom, Probir Chakravarty, James Briscoe, Silvia D M Santos
{"title":"Combinatorial BMP4 and activin direct the choice between alternate routes to endoderm in a stem cell model of human gastrulation.","authors":"Oliver C K Inge, Elias Copin, Jake Cornwall-Scoones, Borzo Gharibi, Irene Rodriguez-Hernandez, Pablo Soro-Barrio, Molly Strom, Probir Chakravarty, James Briscoe, Silvia D M Santos","doi":"10.1016/j.devcel.2025.08.009","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.08.009","url":null,"abstract":"<p><p>Lineage specification requires accurate interpretation of multiple signaling cues. However, how combinatorial signaling histories influence fate outcomes remains unclear. We combined single-cell transcriptomics, live-cell imaging, and mathematical modeling to explore how activin and bone morphogenetic protein 4 (BMP4) guide fate specification during human gastrulation. We see that these signals interact both synergistically and antagonistically to drive fate decisions. We find that definitive endoderm arises from lineage convergence: a direct route from pluripotency and an indirect route via a mesoderm progenitor state. Cells pass through temporal windows of signaling competency, and the relative concentration of activin and BMP4 dictates the trajectory choice. The efficiency between routes is underpinned by a dual role of BMP4 in inducing mesoderm genes while promoting pluripotency exit. This work underscores that the combination of signals a cell is exposed to not only directs its final fate but also the developmental route taken, suggesting lineage convergence enhances robustness in fate specification.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032966","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}
{"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}
Developmental cellPub Date : 2025-09-08DOI: 10.1016/j.devcel.2025.06.023
Yuan Chen
{"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}
Developmental cellPub Date : 2025-09-08DOI: 10.1016/j.devcel.2025.08.008
Ran Lu, Elwira Smakowska-Luzan
{"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}