{"title":"Tumor-intrinsic FDFT1 determines coordinated macrophage anti-tumor immunity.","authors":"Rongchen Shi, Yulan Huang, Pengfei Zheng, Dapeng Zhang, Qing Qin, Fan Zhang, Meng Wang, Kun Zhao, Minli Yang, Xu Guan, Renchao Deng, Hongming Miao","doi":"10.1016/j.devcel.2026.04.003","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.04.003","url":null,"abstract":"<p><p>Macrophage anti-tumor efficacy requires coordinated inflammatory activation and phagocytic function, whether a tumor-intrinsic metabolic regulator simultaneously determines both macrophage anti-tumor mechanisms remains unclear. Here, we screened and identified that farnesyl-diphosphate farnesyltransferase 1 (FDFT1) drives the dual inhibition of macrophage activation and phagocytic function and promotes tumor progression. Mechanistically, tumor-intrinsic FDFT1 directly binds to STAT3 and facilitates the later phosphorylation, which induces PD-L1-dependent suppression of macrophage phagocytosis. Concurrently, FDFT1 binds to and stabilizes cholesterol 25-hydroxylase (CH25H) to promote the secretion of 25-hydroxycholesterol (25HC), suppressing proinflammatory activation of macrophages. Furthermore, FDFT1-mediated dual anti-tumor pathways were validated in mouse tumor models and correlated with clinical pathophysiology. Notably, a small-molecule drug FDFT1-I (2123) targeting FDFT1 inhibits both STAT3-PD-L1 and CH25H/25HC pathways and improves anti-tumor immunity. Collectively, our findings highlight FDFT1 as a tumor-intrinsic metabolic factor promoting tumor development via dual macrophage-dependent mechanisms, suggesting FDFT1 as a promising target for tumor therapy.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811999","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 : 2026-04-28DOI: 10.1016/j.devcel.2026.04.001
Lan Wang, Chris R Harris, Crissy Dudgeon, Orjola Prela, Juliana Cazarin, Ching-Hua Shih, Christina Davidson, Anthony Casabianca, Subhajyoti De, Wade Narrow, Jennifer Becker, Paul M Grandgenett, Michael A Hollingsworth, Jean L Grem, Minsoo Kim, Yeonsun Hong, Scott Gerber, Paula M Vertino, Chongfeng Gao, Zachary Klamer, Anna Repesh, Yansheng Hao, Allison T Ryan, Mitchell Breitenbach, Anna Bianchi, Jashodeep Datta, Brian J Altman, Brian Haab, Darren R Carpizo
{"title":"The circadian gene Dec2 promotes pancreatic cancer progression and dormancy through immune evasion.","authors":"Lan Wang, Chris R Harris, Crissy Dudgeon, Orjola Prela, Juliana Cazarin, Ching-Hua Shih, Christina Davidson, Anthony Casabianca, Subhajyoti De, Wade Narrow, Jennifer Becker, Paul M Grandgenett, Michael A Hollingsworth, Jean L Grem, Minsoo Kim, Yeonsun Hong, Scott Gerber, Paula M Vertino, Chongfeng Gao, Zachary Klamer, Anna Repesh, Yansheng Hao, Allison T Ryan, Mitchell Breitenbach, Anna Bianchi, Jashodeep Datta, Brian J Altman, Brian Haab, Darren R Carpizo","doi":"10.1016/j.devcel.2026.04.001","DOIUrl":"10.1016/j.devcel.2026.04.001","url":null,"abstract":"<p><p>The mechanisms that regulate immune evasion by pancreatic ductal adenocarcinomas (PDACs) remain poorly understood. Using a mouse model of resectable PDAC, we identified an unknown role of the circadian rhythm gene Differentially Expressed in Chondrocytes 2 (Dec2) in regulating tumor progression and dormancy. Deletion of Dec2 from tumor cells substantially increased mouse survival after resection due to an immune-mediated mechanism, as the survival benefit was abrogated under immunodeficient conditions. Dec2 promotes immune evasion by repressing major histocompatibility complex class I (MHC-I)-dependent antigen presentation and by repolarizing the tumor microenvironment from immunologically cold (low T cell infiltration) to hot (elevated T cell infiltration). Dec2 is also a regulator of circadian rhythms, and we found that genes involved in MHC-I antigen presentation and MHC-I surface localization oscillated in a circadian manner, which was lost upon deletion of Dec2 in vitro. We conclude that Dec2 promotes primary PDAC progression and likely metastatic dormancy through immune evasion.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":""},"PeriodicalIF":8.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765530","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 : 2026-04-21DOI: 10.1016/j.devcel.2026.03.010
Silvia Campanario, Mercedes Grima-Terrén, Megan Rommelfanger, Stefania Dell’ Orso, Xuesong Feng, Andrés Cisneros, Ignacio Ramírez-Pardo, Aina Calls-Cobos, Benjamin A. Yang, Kyung Dae Ko, Esther García-Domínguez, Laura Pena-Couso, Grace Chou, Yuewen Zheng, Nasun Hah, Davide Randazzo, Alberto Pérez-Garcia, Tovah E. Markowitz, Jose Milisenda, Iago Pinal-Fernandez, Pura Muñoz-Cánoves
{"title":"A skeletal muscle atlas shows neuromuscular junction adaptations to growth and atrophy","authors":"Silvia Campanario, Mercedes Grima-Terrén, Megan Rommelfanger, Stefania Dell’ Orso, Xuesong Feng, Andrés Cisneros, Ignacio Ramírez-Pardo, Aina Calls-Cobos, Benjamin A. Yang, Kyung Dae Ko, Esther García-Domínguez, Laura Pena-Couso, Grace Chou, Yuewen Zheng, Nasun Hah, Davide Randazzo, Alberto Pérez-Garcia, Tovah E. Markowitz, Jose Milisenda, Iago Pinal-Fernandez, Pura Muñoz-Cánoves","doi":"10.1016/j.devcel.2026.03.010","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.010","url":null,"abstract":"The molecular basis underlying muscle atrophy, as it occurs during disuse or aging, and activity-induced hypertrophy remain poorly understood. A major challenge has been defining the diverse cellular and niche environments within skeletal muscle, which is mostly composed of multinucleated myofibers. Here, we present a single-nucleus and single-cell transcriptomic atlas, coupled with spatial profiling, of mouse limb skeletal muscle under resting conditions and during experimentally induced atrophy or hypertrophy. We identify condition-dependent shifts in muscle-resident cell populations and fiber-type-specific transcriptional responses. We also uncover extensive remodeling of the neuromuscular junction (NMJ), including the emergence of specialized synaptic myonuclei (SynM) and terminal Schwann cells (tSCs) associated with atrophic or hypertrophic states. High-resolution 3D imaging and spatial transcriptomics confirm these changes at the tissue level. Similar NMJ alterations are observed in denervated and exercised human muscle, supporting the translational relevance of this atlas for studying muscle plasticity and identifying therapeutic targets in muscle-related diseases.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"136 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726414","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 : 2026-04-13DOI: 10.1016/j.devcel.2026.03.008
Irene Basili, Francesca Bufalieri, Marilisa Conenna, Shirin Navacci, Yue-Ru Li, Jacob Torrejon, Flavia Bernardi, Ludovica Lospinoso Severini, Veronique Marsaud, Gabriele Cancila, Guillaume Bourmeau, Hua Yu, Valentina Lo Re, Julie Talbot, Gennaro Adabbo, Alberico Di Pinto, Francesca Agnoli, Daniela Giovannini, Simona Leonardi, Rosa Bordone, Lucia Di Marcotullio
{"title":"AMBRA1 enhances Sonic Hedgehog signaling during cerebellar development and in medulloblastoma","authors":"Irene Basili, Francesca Bufalieri, Marilisa Conenna, Shirin Navacci, Yue-Ru Li, Jacob Torrejon, Flavia Bernardi, Ludovica Lospinoso Severini, Veronique Marsaud, Gabriele Cancila, Guillaume Bourmeau, Hua Yu, Valentina Lo Re, Julie Talbot, Gennaro Adabbo, Alberico Di Pinto, Francesca Agnoli, Daniela Giovannini, Simona Leonardi, Rosa Bordone, Lucia Di Marcotullio","doi":"10.1016/j.devcel.2026.03.008","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.008","url":null,"abstract":"AMBRA1 (autophagy and beclin 1 regulator 1) is primarily recognized as a tumor suppressor. However, its role as a tumor promoter has garnered increasing attention. Here, leveraging clinical data of an international multi-omic medulloblastoma (MB) cohort, we identified that elevated AMBRA1 protein levels, independently of its mRNA expression, correlate with poor prognosis in the Sonic Hedgehog subgroup (MB<sub>SHH</sub>). Mechanistically, AMBRA1 enhances SHH signaling by stabilizing GLI1, the pathway’s final effector, via inhibition of its βTrCP-mediated degradation. Additionally, AMBRA1 protein stability is modulated by the REN E3 ubiquitin ligase, a tumor suppressor gene lost in MB<sub>SHH</sub>. Inhibition of AMBRA1 blocks MB<sub>SHH</sub> growth in murine and patient-derived preclinical models. Moreover, combining <em>AMBRA1</em> knockdown with FDA-approved SHH inhibitors enhances antitumor efficacy. These findings identify the AMBRA1/βTrCP/REN axis as a key regulatory mechanism in SHH signaling and discover an unrecognized function of AMBRA1 in MB<sub>SHH</sub>, providing actionable insights into brain tumor biology.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"5 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147666430","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 : 2026-04-08Epub Date: 2026-02-19DOI: 10.1016/j.devcel.2026.01.015
Anna Stephan, Flavia A Graca, Vishwajeeth R Pagala, Liam C Hunt, Chia-Lung Chuang, John Grime, Daniel Alford, Xusheng Wang, Anthony A High, Junmin Peng, Fabio Demontis
{"title":"Insolubilome profiling defines molecular features that influence protein insolubility with aging.","authors":"Anna Stephan, Flavia A Graca, Vishwajeeth R Pagala, Liam C Hunt, Chia-Lung Chuang, John Grime, Daniel Alford, Xusheng Wang, Anthony A High, Junmin Peng, Fabio Demontis","doi":"10.1016/j.devcel.2026.01.015","DOIUrl":"10.1016/j.devcel.2026.01.015","url":null,"abstract":"<p><p>Solubility regulates protein function, but how it is governed by aging remains elusive. Here, we utilized mass spectrometry to define the relative composition of the soluble and insoluble tissue/organ fractions during mouse aging. In the young, there is a wide (∼100-1,000×) range of insoluble/soluble protein ratios that differ tissue-specifically. With aging, some proteins become relatively more insoluble, while others are conversely regulated or unaffected. Age-related insoluble/soluble changes are not merely dictated by histological similarity, diverge in related tissues with distinct degeneration propensities, and correlate tissue-specifically with structural features. Proteins that become age-insoluble in multiple organs include aggregation-prone circulating factors and ectopically expressed proteins. For instance, although primarily expressed by the epidermis, hornerin insolubility increases with aging in skeletal muscle, and experimental hornerin upregulation causes muscle weakness. Thus, age-insoluble proteins are useful biomarkers but can also contribute to age-related functional decline, highlighting a multifaceted remodeling of the insolubilome with aging.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"936-958.e7"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257717","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 : 2026-04-08Epub Date: 2026-02-05DOI: 10.1016/j.devcel.2026.01.006
Tommaso Ristori, Raphael Thuret, Erika Hooker, Peter Quicke, Sami Sanlidag, Kevin Lanthier, Kalonji Ntumba, Irene M Aspalter, Marina Uroz, Cecilia M Sahlgren, Shane P Herbert, Christopher S Chen, Bruno Larrivée, Katie Bentley
{"title":"Bmp9 regulates Notch signaling and the temporal dynamics of angiogenesis via Lunatic Fringe.","authors":"Tommaso Ristori, Raphael Thuret, Erika Hooker, Peter Quicke, Sami Sanlidag, Kevin Lanthier, Kalonji Ntumba, Irene M Aspalter, Marina Uroz, Cecilia M Sahlgren, Shane P Herbert, Christopher S Chen, Bruno Larrivée, Katie Bentley","doi":"10.1016/j.devcel.2026.01.006","DOIUrl":"10.1016/j.devcel.2026.01.006","url":null,"abstract":"<p><p>Sprouting angiogenesis and blood vessel stabilization require precise coordination between endothelial cells (ECs) and pericytes. Bone Morphogenic Protein 9 (Bmp9), whose signaling through activin receptor-like kinase 1 (Alk1) is dysregulated in several diseases, was thought to regulate these processes by independently activating Notch target genes in an additive fashion with canonical Notch signaling. Here, through predictive computational modeling validated in mice, zebrafish, and human cell lines, we uncover that Bmp9 enhances Notch activity synergistically by upregulating Lunatic Fringe (Lfng) in ECs. Specifically, Bmp9-induced Lfng enhances Notch receptor activation, most strongly when Delta-like ligand 4 (Dll4) is also present. This Lfng regulation alters vessel branching by modulating the timing of EC phenotype selection and rearrangement during angiogenesis. Lfng also contributes to pericyte-driven vessel stabilization by mediating Jagged1 upregulation in Bmp9-stimulated ECs. In summary, Bmp9-upregulated Lfng enhances Dll4-Notch1 signaling in ECs and Jag1-Notch3 activation in pericytes, shaping angiogenic sprouting and stabilization outcomes.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"837-853.e9"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131489","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 : 2026-04-08DOI: 10.1016/j.devcel.2026.03.002
Wenxin Zhang, Junren Dai, Ying Hu
{"title":"Lysosomal rupture: An emerging switch for collective ferroptosis.","authors":"Wenxin Zhang, Junren Dai, Ying Hu","doi":"10.1016/j.devcel.2026.03.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.002","url":null,"abstract":"<p><p>Ferroptosis can propagate collectively between cells. In this issue of Developmental Cell, Das et al.<sup>1</sup> report that glutathione (GSH) depletion converts glutathione peroxidase 4 (GPX4)-inhibition-induced ferroptosis from a single-cell to a collective fate, and confirms the central role of lysosomal rupture in this process.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"61 4","pages":"709-710"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644624","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 : 2026-04-08DOI: 10.1016/j.devcel.2026.03.004
Li Li, Anca M Pasca
{"title":"Non-canonical roles for Hif-1α in interneuron progenitor proliferation and cortical circuit maturation.","authors":"Li Li, Anca M Pasca","doi":"10.1016/j.devcel.2026.03.004","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.004","url":null,"abstract":"<p><p>In this issue of Developmental Cell, Lu et al. reveal that Hif-1α plays a non-canonical role in cortical interneuron development and interacts with Grin2b, a gene associated with neurodevelopmental disorders.<sup>1</sup> The study highlights that controlled Hif-1α expression is essential for brain development yet achievable without activating the hypoxia-response pathway.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"61 4","pages":"713-715"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644611","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":"AVP1-mediated pyrophosphate homeostasis coordinates calcium-dependent cellulose synthesis and autoimmunity during leaf growth.","authors":"Chen Fu, Zhihang Feng, Xu Teng, Yusuke Shikanai, Shuichi Hashimoto, Takehiro Kamiya, Zhiyi Jia, Wenjian Song, Yihui Xiao, Huiting Chen, Mutsumi Yamagami, Shinichiro Sawa, Yan Liang, Xiaobo Zhao, Xianyong Lin, Weiming Shi, Wolfgang Busch, Toru Fujiwara, Baohai Li","doi":"10.1016/j.devcel.2026.01.005","DOIUrl":"10.1016/j.devcel.2026.01.005","url":null,"abstract":"<p><p>Calcium (Ca) availability is vital for optimal plant growth and immune signaling, yet the underlying mechanisms remain elusive. Here, we reveal that Arabidopsis vacuolar H⁺-pyrophosphatase (AVP1)-regulated cytosolic inorganic pyrophosphate (PPi) homeostasis governs leaf growth by maintaining cellulose synthesis to suppress autoimmune activation upon Ca deficiency. Ca deficiency reduces the AVP1 abundance, while AVP1 eliminates excess cytosolic PPi, which impairs guanosine triphosphate-dependent microtubule assembly and reduces cellulose synthase 3-mediated cellulose synthesis. This cell-wall disruption activates isochorismate synthase 1-mediated salicylic acid production, triggering autoimmune responses and inhibiting new leaf growth. Enhancing PPi hydrolysis genetically improves plant growth tolerance to low Ca availability (low-Ca). The link between Ca-dependent PPi metabolic regulation, autoimmunity, and leaf growth is conserved in tomato, highlighting the broad relevance of AVP1 and PPi homeostasis in plant resilience. Our findings offer potential strategies for improving crop tolerance to nutrient-limited environments.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"820-836.e9"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131404","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 : 2026-04-08DOI: 10.1016/j.devcel.2026.02.019
Oluwatoyosi M Adaramodu, Brian D Gregory
{"title":"A lineage-specific autophagic mechanism of P-body turnover.","authors":"Oluwatoyosi M Adaramodu, Brian D Gregory","doi":"10.1016/j.devcel.2026.02.019","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.02.019","url":null,"abstract":"<p><p>Processing bodies (P-bodies) are cytoplasmic RNA granules that assemble and dissolve as cells adjust gene expression; however, mechanisms that control their turnover in eukaryotic organisms are unclear. In this issue of Developmental Cell, Abdrakhmanov et al. demonstrate that P-bodies are degraded in Marchantia polymorpha via the direct interaction of the decapping proteins EDC4 and DCP1 with the autophagy receptor ATG8.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"61 4","pages":"707-708"},"PeriodicalIF":8.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644538","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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