Cell reports最新文献_第3页

Hedgehog-driven adaxial cell constriction patterns slow muscle fate and somite boundary remodeling in the presomitic mesoderm. 刺猬驱动的近轴细胞收缩模式减缓了体前中胚层的肌肉命运和体体边界重塑。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-29 DOI: 10.1016/j.celrep.2026.117319

Yawen Wang, Xiang Li, Rui Xia, Yinan Wan, Jingao Lu, Zhonghua Zhao, Wenqing Zhang, Qiang Wang, Timothy E Saunders, Jianmin Yin

{"title":"Hedgehog-driven adaxial cell constriction patterns slow muscle fate and somite boundary remodeling in the presomitic mesoderm.","authors":"Yawen Wang, Xiang Li, Rui Xia, Yinan Wan, Jingao Lu, Zhonghua Zhao, Wenqing Zhang, Qiang Wang, Timothy E Saunders, Jianmin Yin","doi":"10.1016/j.celrep.2026.117319","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117319","url":null,"abstract":"How morphogen signaling interfaces with cell behaviors and mechanics to coordinate body axis patterning has remained largely unclear. Here, we uncover a mechanochemical program that directs slow muscle fate commitment and somite boundary remodeling in the presomitic mesoderm (PSM). Hedgehog, secreted from the underlying notochord, triggers cytoskeletal remodeling and basal constriction in adaxial cells, progressively reducing notochord contact and allowing adjacent cells to engage the morphogen source. Concurrently, directional rearrangements of dorsal and ventral medial cells shift prospective somite boundaries posteriorly, converting straight borders into V-shaped patterns before segmentation. Vertex modeling and mutant analyses indicate that Hedgehog-dependent constriction of adaxial cells initiates the tissue deformation, while somite segmentation stabilizes this architecture. Using an integrative multi-omics approach with targeted gene validation, we identified acta1a (a major skeletal muscle actin isoform) and arhgef25a (a RhoGEF) as key participants in adaxial cell morphogenesis in the PSM.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117319"},"PeriodicalIF":6.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811673","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}

引用次数: 0

HCMV infection depends on EGLN1-mediated mitochondrial activation to increase dNTP pools for viral DNA replication. HCMV感染依赖于egln1介导的线粒体激活来增加病毒DNA复制的dNTP池。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-29 DOI: 10.1016/j.celrep.2026.117329

Lucas A Simpson, Diana M Dunn, Wyatt Fales, Zachary J Moore, Jessica H Ciesla, Nicole C Waild, Matthew H Raymonda, Isaac S Harris, Joshua Munger

{"title":"HCMV infection depends on EGLN1-mediated mitochondrial activation to increase dNTP pools for viral DNA replication.","authors":"Lucas A Simpson, Diana M Dunn, Wyatt Fales, Zachary J Moore, Jessica H Ciesla, Nicole C Waild, Matthew H Raymonda, Isaac S Harris, Joshua Munger","doi":"10.1016/j.celrep.2026.117329","DOIUrl":"10.1016/j.celrep.2026.117329","url":null,"abstract":"Human cytomegalovirus (HCMV) is a leading cause of congenital infection and morbidity in immunosuppressed populations. Like all viruses, HCMV is an obligate intracellular parasite that extensively remodels host cell metabolism to support its replication, yet the precise underlying mechanisms and the potentially associated metabolic vulnerabilities remain poorly understood. Using a metabolism-focused screening platform, we identify EGLN prolyl hydroxylase activity as critical for HCMV infection. Our studies reveal that HCMV infection depends on EGLN1, which accumulates in mitochondria during infection. Inhibition of EGLN1 expression blocks HCMV-mediated mitochondrial activation, which in turn prevents the production of the deoxynucleoside triphosphate (dNTP) precursors necessary for dNTP pool expansion and viral DNA replication. Further, pharmacological EGLN inhibition attenuates viral infection in a humanized mouse model. Collectively, these data establish EGLN1 as a critical determinant of mitochondrial metabolic remodeling and virally-induced dNTP generation during HCMV infection, highlighting EGLN1 as a promising antiviral therapeutic target.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117329"},"PeriodicalIF":6.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811684","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}

引用次数: 0

MELK inhibition promotes megakaryopoiesis and platelet recovery in models of immune thrombocytopenia through ERK/cofilin signaling. MELK抑制通过ERK/cofilin信号传导促进免疫性血小板减少模型的巨核生成和血小板恢复。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-29 DOI: 10.1016/j.celrep.2026.117339

Xueqian Li, Jiaqian Qi, Tiantian Chu, Qixiu Hou, Haohao Han, Ziyan Zhang, Meng Zhou, Hong Wang, Siyi Lu, Depei Wu, Yue Han

{"title":"MELK inhibition promotes megakaryopoiesis and platelet recovery in models of immune thrombocytopenia through ERK/cofilin signaling.","authors":"Xueqian Li, Jiaqian Qi, Tiantian Chu, Qixiu Hou, Haohao Han, Ziyan Zhang, Meng Zhou, Hong Wang, Siyi Lu, Depei Wu, Yue Han","doi":"10.1016/j.celrep.2026.117339","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117339","url":null,"abstract":"Dysregulated megakaryocyte (MK) maturation is a key feature of immune thrombocytopenia (ITP), yet the specific mechanisms and targeted molecules remain elusive. This study identifies the serine/threonine kinase maternal embryonic leucine zipper kinase (MELK) as a potential regulator of megakaryopoiesis in ITP. MELK expression is significantly elevated in bone marrow MKs of patients with ITP compared with healthy donors and inversely correlates with platelet counts. Functionally, inhibition of MELK not only promotes MK maturation in vitro but also promotes platelet recovery in the ITP mouse model. Mechanistic studies reveal that MELK modulates megakaryopoiesis through the MAPK/ERK pathway. Confocal microscopy and western blot verifications indicate that MELK inhibition reduces cofilin phosphorylation, thereby positively regulating cytoskeletal dynamics, and this effect is abrogated by MAPK/ERK blocking. These findings suggest that MELK inhibition promotes MK maturation and platelet production via the MAPK/ERK/cofilin axis, providing a potential for the development of therapeutic options for ITP.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117339"},"PeriodicalIF":6.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811616","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}

引用次数: 0

Motif grammar and transcriptional programs decouple CTCF binding from nucleosome phasing to control cell-type-specific chromatin insulation. 基序语法和转录程序从核小体相位解耦CTCF结合，以控制细胞类型特异性染色质绝缘。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-29 DOI: 10.1016/j.celrep.2026.117316

Catherine Do, Guimei Jiang, Paul Zappile, Adriana Heguy, Jane A Skok

{"title":"Motif grammar and transcriptional programs decouple CTCF binding from nucleosome phasing to control cell-type-specific chromatin insulation.","authors":"Catherine Do, Guimei Jiang, Paul Zappile, Adriana Heguy, Jane A Skok","doi":"10.1016/j.celrep.2026.117316","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117316","url":null,"abstract":"CTCF organizes the genome via cohesin-mediated loop extrusion, insulating topologically associating domains (TADs) and constraining enhancer-promoter communication. Yet, CTCF binding varies across cell types and genomic contexts. In mouse, typically accessible sites combine strong motifs with higher CTCF/cohesin occupancy, while inaccessible sites use weaker motifs stabilized by flanking upstream (U) and downstream (D) sequences that engage peripheral zinc fingers to respectively enhance or dampen binding. Notably, TF motifs within ±35 bp bind cooperatively or competitively depending on expression and positional overlap, a finding supported by AlphaFold predictions and allele-specific perturbations. Favorable motif/TF environments can increase CTCF signal yet disrupt nucleosome phasing and weaken insulation, showing that binding strength and insulation can be uncoupled. Single-molecule maps show that nucleosome phasing regularity predicts insulation strength more reliably than CTCF peak intensity. Thus, differences in motif architecture and TF abundance between species and cell states provide a mechanism for cell-type-specific regulation of CTCF-mediated chromatin insulation.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117316"},"PeriodicalIF":6.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811676","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}

引用次数: 0

Artificial intelligence-driven donor-recipient gut microbiome matching for optimized fecal microbiota transplantation. 人工智能驱动的供受体肠道微生物组匹配优化粪便微生物群移植。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-29 DOI: 10.1016/j.celrep.2026.117301

Qi Su, Sizhe Chen, Louis Hs Lau, Rashid N Lui, Yun Wang, Zhilu Xu, Chun Pan Cheung, Jessica Y L Ching, Xiaotao Shen, Ye Peng, Hein Min Tun, Gianluca Ianiro, David Rubin, Eugene B Chang, Francis Ka Leung Chan, Siew Chien Ng

{"title":"Artificial intelligence-driven donor-recipient gut microbiome matching for optimized fecal microbiota transplantation.","authors":"Qi Su, Sizhe Chen, Louis Hs Lau, Rashid N Lui, Yun Wang, Zhilu Xu, Chun Pan Cheung, Jessica Y L Ching, Xiaotao Shen, Ye Peng, Hein Min Tun, Gianluca Ianiro, David Rubin, Eugene B Chang, Francis Ka Leung Chan, Siew Chien Ng","doi":"10.1016/j.celrep.2026.117301","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117301","url":null,"abstract":"Fecal microbiota transplantation (FMT) has emerged as a promising therapy for gastrointestinal diseases, yet its clinical efficacy remains individually variable. Here, we analyze multi-kingdom and functional profiles in pre- and post-FMT metagenomes from 515 FMTs across 30 cohorts and 12 diseases, in which 94 metagenomes from 44 FMTs are newly collected. We reveal a robust association between clinical efficacy and post-FMT microbiome convergence of recipients toward donors, across diseases. To predict post-FMT microbial convergence, we develop MOZAIC (Microbiome Matching Optimization via Artificial Intelligence), a framework that integrates multi-dimensional donor-recipient microbiota features. MOZAIC achieves an average area under the curve (AUC) of 0.88 and accuracy/recall >0.80 in forecasting microbiome convergence, with 78.7% accuracy in predicting clinical outcomes, and retrospectively simulates a 1.44-fold improvement (from 49.4% to 71.0%) in clinical response rates over baseline. This study establishes microbiome convergence as a key mediator of FMT and provides a scalable tool for precision matching in microbiota-based therapies.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":" ","pages":"117301"},"PeriodicalIF":6.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811613","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}

引用次数: 0

Proteomic and lipidomic analyses reveal molecular subtypes and potential targets in early-stage lung adenocarcinoma among non-smokers. 蛋白质组学和脂质组学分析揭示了非吸烟者早期肺腺癌的分子亚型和潜在靶点。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-28 DOI: 10.1016/j.celrep.2026.117215

Yaohui Sun, Jian Liu, Xin Xu, Qiqi Liu, Hua Cheng, Wenwen Huo, Ronghao Wang, Qingdong Cao

{"title":"Proteomic and lipidomic analyses reveal molecular subtypes and potential targets in early-stage lung adenocarcinoma among non-smokers.","authors":"Yaohui Sun, Jian Liu, Xin Xu, Qiqi Liu, Hua Cheng, Wenwen Huo, Ronghao Wang, Qingdong Cao","doi":"10.1016/j.celrep.2026.117215","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117215","url":null,"abstract":"Early-stage lung adenocarcinoma (LUAD) in never smokers exhibits distinct biological features, yet the metabolic programs driving early invasion remain unclear. We integrate proteomic and lipidomic profiling of primary LUAD tumors from never smokers, matched normal adjacent tissues (NATs), and benign pulmonary nodules (BPNs). Integrated multi-omics analysis reveals coordinated dysregulation of lipid metabolism and immune signaling in early LUAD. Proteome-based network fusion stratifies invasive LUAD into immune-metabolic synergistic (IMS) and metabolic-stress-driven (MSD) subtypes. IMS tumors retain apolipoprotein-associated lipid modules and favorable immune features, whereas MSD tumors exhibit stress-response programs. Mechanistically, APOA1 and APOC1 emerge as key nodes linking lipid homeostasis to invasion, and their depletion promotes LUAD cell migration and invasion. We establish a two-protein, four-lipid diagnostic panel demonstrating robust performance across tissue and plasma cohorts. These findings provide a molecular basis for early detection and risk stratification in never smokers.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117215"},"PeriodicalIF":6.9,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763611","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}

引用次数: 0

USP15 stabilizes c-Myc to drive sunitinib resistance by suppressing cuproptosis in clear cell renal cell carcinoma. USP15稳定c-Myc，通过抑制透明细胞肾细胞癌中的铜增生来驱动舒尼替尼耐药性。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-28 DOI: 10.1016/j.celrep.2026.117328

Yujie Chen, Shiyu Huang, Lei Wang, Zhiyuan Yao, Shujie Fu, Juncheng Hu, Xiuheng Liu, Zhiyuan Chen

{"title":"USP15 stabilizes c-Myc to drive sunitinib resistance by suppressing cuproptosis in clear cell renal cell carcinoma.","authors":"Yujie Chen, Shiyu Huang, Lei Wang, Zhiyuan Yao, Shujie Fu, Juncheng Hu, Xiuheng Liu, Zhiyuan Chen","doi":"10.1016/j.celrep.2026.117328","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117328","url":null,"abstract":"Cuproptosis, a recently characterized form of mitochondrial-dependent cell death triggered by copper accumulation, remains unexplored in clear cell renal cell carcinoma (ccRCC) and sunitinib resistance. Here, we reveal that the deubiquitinase USP15 suppressed cuproptosis and drove sunitinib resistance in ccRCC. Mechanistically, USP15 stabilized c-Myc through K48-linked deubiquitination at K143 and K289, leading to transcriptional upregulation of PDK1, PDK3, and PDK4 and subsequent repression of DLAT expression and pyruvate dehydrogenase, thereby conferring resistance to cuproptosis. Conversely, the E3 ligase MYCBP2 promoted K48-linked ubiquitination and degradation of c-Myc, antagonizing USP15 function. Sunitinib treatment induced features of cuproptosis, while USP15 upregulation in resistant cells suppressed these effects. USP15 depletion or elesclomol (ES)-Cu/disulfiram (DSF)-Cu restored sunitinib sensitivity both in vitro and vivo without systemic toxicity. Collectively, our findings identify USP15 as a critical regulator of cuproptosis and sunitinib resistance and highligh cuproptosis activation as a promising strategy to overcome tyrosine kinase inhibitor (TKI) resistance in ccRCC.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117328"},"PeriodicalIF":6.9,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763723","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}

引用次数: 0

The long isoform of ZAP coordinates multiple enzymes to mediate complete decay of target transcripts. ZAP的长同种异构体协调多种酶介导目标转录物的完全衰变。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-28 DOI: 10.1016/j.celrep.2026.117305

Clément R Bouton, Grega Gimpelj Domjanič, María José Lista, Rui Pedro Galão, Thomas Courty, Piotr Kwiatkowski, Harry D Wilson, Peter W S Hill, Hannah E Mischo, Anob M Chakrabarti, Mario Poljak, Jernej Ule, Stuart J D Neil, Chad M Swanson

{"title":"The long isoform of ZAP coordinates multiple enzymes to mediate complete decay of target transcripts.","authors":"Clément R Bouton, Grega Gimpelj Domjanič, María José Lista, Rui Pedro Galão, Thomas Courty, Piotr Kwiatkowski, Harry D Wilson, Peter W S Hill, Hannah E Mischo, Anob M Chakrabarti, Mario Poljak, Jernej Ule, Stuart J D Neil, Chad M Swanson","doi":"10.1016/j.celrep.2026.117305","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117305","url":null,"abstract":"Zinc-finger antiviral protein (ZAP)-mediated RNA decay (ZMD) restricts the replication of viruses containing CpG dinucleotide clusters. However, why ZAP isoforms differ in antiviral activity and how they recruit cofactors to mediate RNA decay is unclear. Therefore, we determined the ordered events of the ZMD pathway. The long ZAP isoform preferentially binds viral RNA and has distinct binding motifs compared to the short isoform. The endoribonuclease KHNYN then cleaves viral RNA at positions of ZAP binding. The 5' cleavage fragment undergoes TUT4/TUT7-mediated 3' uridylation and degradation by DIS3L2. The 3' cleavage fragment is degraded by XRN1. ZAP and TRIM25 interact with KHNYN, TUT7, DIS3L2, and XRN1 in an RNase-resistant manner. Viral infection promotes the interaction between TRIM25 with these enzymes, leading to viral RNA decay while also decreasing the abundance of cellular transcripts. Overall, the long isoform of ZAP recruits key enzymes to assemble an RNA decay complex on viral RNA.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117305"},"PeriodicalIF":6.9,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763680","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}

引用次数: 0

Heat shock protein 90β lactylation acts as a metabolic switch to drive cerebrovascular apoptosis under heat stress. 热休克蛋白90β乳酸化作为代谢开关，在热应激下驱动脑血管凋亡。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-27 DOI: 10.1016/j.celrep.2026.117317

Jirui Wen, Yuhao Zou, Can Li, Ling Wang, Zhengdong Lin, Juan Cheng, Tianshan Zhang, Zhizhen Hao, Shixi Liu, Xuehong Wan, Rong Yao, Jifeng Liu, Jiang Wu

{"title":"Heat shock protein 90β lactylation acts as a metabolic switch to drive cerebrovascular apoptosis under heat stress.","authors":"Jirui Wen, Yuhao Zou, Can Li, Ling Wang, Zhengdong Lin, Juan Cheng, Tianshan Zhang, Zhizhen Hao, Shixi Liu, Xuehong Wan, Rong Yao, Jifeng Liu, Jiang Wu","doi":"10.1016/j.celrep.2026.117317","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117317","url":null,"abstract":"Lysine lactylation (Kla) is a metabolite-sensing post-translational modification that bridges cellular metabolism to protein function. Here, we discover that heat stress triggers anaerobic glycolysis and lactate accumulation in brain microvascular endothelial cells. We find that plasma lactate inversely correlates with Glasgow Coma Scale scores in heat stroke patients and predicts poor outcomes. Mechanistically, AARS1 catalyzes the transfer of lactate to HSP90β at lysine 275 (K275). Critically, the lactylation of HSP90β disrupts its interaction with apoptotic protease-activating factor 1 (APAF-1). This modification compromises the protective function of HSP90β, liberating APAF-1 to activate the mitochondrial apoptosis pathway, resulting in blood-brain barrier (BBB) injury. Functional validation reveals that decreasing lactate production or inhibiting AARS1 confers protection. These findings establish HSP90β K275 lactylation as a metabolic switch that modulates protective mechanisms during heat stress-induced cerebrovascular injury. Collectively, our study provides insights into heat stress pathogenesis and identifies potential therapeutic targets for heat-related brain damage.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117317"},"PeriodicalIF":6.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763796","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}

引用次数: 0

BIN2 phosphorylation of GRF5 suppresses low-nitrate root foraging by inhibiting transcriptional activity and UBP12/13-mediated deubiquitination. GRF5的BIN2磷酸化通过抑制转录活性和ubp12 /13介导的去泛素化来抑制低硝酸盐根的觅食。

IF 6.9 1区生物学

Cell reports Pub Date : 2026-04-27 DOI: 10.1016/j.celrep.2026.117323

Taotao Li, Xiuhong Yao, Dongxiao Liu, Xinke Kang, Ke Fang, Mei Zhao, Yuqing Zhao, Yueli Cai, Jingjing Sun, Wenhui Tian, Luping Gong, Zhenjiang Wu, Wenxi Wei, Mengyuan Li, Chunli Liao, Lianzhe Wang, Honghui Lin, Dawei Zhang

{"title":"BIN2 phosphorylation of GRF5 suppresses low-nitrate root foraging by inhibiting transcriptional activity and UBP12/13-mediated deubiquitination.","authors":"Taotao Li, Xiuhong Yao, Dongxiao Liu, Xinke Kang, Ke Fang, Mei Zhao, Yuqing Zhao, Yueli Cai, Jingjing Sun, Wenhui Tian, Luping Gong, Zhenjiang Wu, Wenxi Wei, Mengyuan Li, Chunli Liao, Lianzhe Wang, Honghui Lin, Dawei Zhang","doi":"10.1016/j.celrep.2026.117323","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117323","url":null,"abstract":"Root developmental plasticity enables plants to adapt to nutrient-deficient conditions. Under low-nitrate (LN) conditions, enhanced exploratory root growth-characterized by increased primary and lateral root (LR) elongation-facilitates nutrient foraging. Although nitrate-hormone crosstalk regulates this process, the underlying molecular mechanisms remain poorly understood. Here, we identify the BIN2-GRF5-UBP12/13 module that governs root foraging responses to LN in Arabidopsis. We demonstrate that BIN2 phosphorylates GRF5 at Ser205, thereby reducing its stability and transcriptional activity. Integrative DAP-seq and transcriptomic analyses reveal that GRF5 directly regulates key nitrate-responsive genes, including the dual-affinity transporter gene NRT1.1 and the high-affinity uptake gene NRT2.1. Furthermore, dephosphorylated GRF5 preferentially interacts with UBIQUITIN-SPECIFIC PROTEASES 12 and 13 (UBP12/13), which stabilizes GRF5 and promotes LR elongation under LN conditions. Our findings delineate a phosphorylation-dependent regulatory circuit that fine-tunes root foraging adaptation, advancing the mechanistic understanding of nitrate sensing in plants.","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 5","pages":"117323"},"PeriodicalIF":6.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763775","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}

引用次数: 0