Developmental cellPub Date : 2024-12-31DOI: 10.1016/j.devcel.2024.12.012
Daxiao Sun, Xueping Zhao, Tina Wiegand, Cecilie Martin-Lemaitre, Tom Borianne, Lennart Kleinschmidt, Stephan W. Grill, Anthony A. Hyman, Christoph Weber, Alf Honigmann
{"title":"Assembly of tight junction belts by ZO1 surface condensation and local actin polymerization","authors":"Daxiao Sun, Xueping Zhao, Tina Wiegand, Cecilie Martin-Lemaitre, Tom Borianne, Lennart Kleinschmidt, Stephan W. Grill, Anthony A. Hyman, Christoph Weber, Alf Honigmann","doi":"10.1016/j.devcel.2024.12.012","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.012","url":null,"abstract":"Tight junctions play an essential role in sealing tissues, by forming belts of adhesion strands around cellular perimeters. Recent work has shown that the condensation of ZO1 scaffold proteins is required for tight junction assembly. However, the mechanisms by which junctional condensates initiate at cell-cell contacts and elongate around cell perimeters remain unknown. Combining biochemical reconstitutions and live-cell imaging of MDCKII tissue, we found that tight junction belt formation is driven by adhesion receptor-mediated ZO1 surface condensation coupled to local actin polymerization. Adhesion receptor oligomerization provides the signal for surface binding and local condensation of ZO1 at the cell membrane. Condensation produces a molecular scaffold that selectively enriches junctional proteins. Finally, ZO1 condensates directly facilitate local actin polymerization and filament bundling, driving the elongation into a continuous tight junction belt. More broadly, our work identifies how cells couple surface condensation with cytoskeleton organization to assemble and structure adhesion complexes.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"1 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142905041","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 : 2024-12-31DOI: 10.1016/j.devcel.2024.12.015
Alexandra L. Nguyen, Eric M. Smith, Iain M. Cheeseman
{"title":"Co-essentiality analysis identifies PRR12 as a cohesin interacting protein and contributor to genomic integrity","authors":"Alexandra L. Nguyen, Eric M. Smith, Iain M. Cheeseman","doi":"10.1016/j.devcel.2024.12.015","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.015","url":null,"abstract":"The cohesin complex is critical for genome organization and regulation, relying on specialized co-factors to mediate its diverse functional activities. Here, by analyzing patterns of similar gene requirements across cell lines, we identify PRR12 as a mediator of cohesin and genome integrity. We show that PRR12 interacts with NIPBL/MAU2 and the cohesin complex, and that the loss of PRR12 results in reduced cohesin localization and a substantial increase in DNA double-strand breaks in mouse NIH-3T3 cells. Additionally, PRR12 co-localizes with NIPBL to sites of DNA damage in a NIPBL and cohesin-dependent manner. We find that the requirement for PRR12 differs across cell lines, with human HeLa cells exhibiting reduced sensitivity to PRR12 loss compared with mouse NIH-3T3 cells, indicating context-specific roles. Together, our work identifies PRR12 as a regulator of cohesin and provides insight into how genome integrity is maintained across diverse cellular contexts.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"48 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142905047","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":"The de novo synthesis of GABA and its gene regulatory function control hepatocellular carcinoma metastasis","authors":"Li Li, Youli Kang, Running Cheng, Fangming Liu, Fujia Wu, Zizhao Liu, Junjie Kou, Zhenxi Zhang, Wei Li, Haitao Zhao, Xiaojing He, Wenjing Du","doi":"10.1016/j.devcel.2024.12.007","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.007","url":null,"abstract":"The neurotransmitter gamma-aminobutyric acid (GABA) has been thought to be involved in the development of some types of cancer. Yet, the <em>de novo</em> synthesis of GABA and how it functions in hepatocellular carcinoma (HCC) remain unclear. Here, we report that SLC6A12 acts as a transporter of GABA, and that aldehyde dehydrogenase 9 family member A1 (ALDH9A1), not glutamate decarboxylase 1 (GAD1), generates GABA in human HCC. Interestingly, SLC6A12 and ALDH9A1 are upregulated during lung metastases of HCC, and depletion of either of them leads to impaired HCC metastasis. Mechanistically, GABA directly binds and stabilizes β-catenin, resulting in activated Wnt/β-catenin signaling, and thereby enhancing HCC metastasis. Reciprocally, β-catenin transcriptionally upregulates SLC6A12 to import more GABA to stabilize β-catenin. Thus, our findings identify ALDH9A1 as the major GABA synthetase in HCC, demonstrate a positive-feedback regulatory mechanism for sustaining Wnt/β-catenin signaling, and reveal a role for β-catenin in sensing GABA, which contributes to HCC metastasis.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"21 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901670","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":"Strigolactone promotes cotton fiber cell elongation by de-repressing DWARF53 on linolenic acid biosynthesis","authors":"Huiqin Wang, Liping Zhu, Mengyuan Fan, Shuangshuang Weng, Xin Zhou, Hanxuan Zhao, Yongcui Shen, Jiaquan Chai, Liyong Hou, Miaomiao Hao, Rezwan Tanvir, Ling Li, Guanghui Xiao","doi":"10.1016/j.devcel.2024.12.009","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.009","url":null,"abstract":"Strigolactone (SL) is a plant hormone required for plant development. DWARF53 (D53) functions as a transcription repressor in SL signaling. However, the role of D53 in cotton (<em>Gossypium hirsutum</em>, Gh) fiber development remains unclear. Here, we identify that GhD53 suppresses fiber elongation by repressing transcription of <em>GhFAD3</em> genes, which control linolenic acid (C18:3) biosynthesis. Mechanistically, GhD53 interacts with SL-related transcriptional activate factor (GhSLRF) to prevent its binding on Omega-3 fatty acid desaturase gene (<em>GhFAD3</em>) promoters, thereby inhibiting <em>GhFAD3</em> transcription. Upon SL exposure, GhD53 is degraded and leads to GhSLRF activation. This activation further promotes <em>GhFAD3</em> transcription, C18:3 biosynthesis, and fiber elongation. Our findings identify the molecular mechanism of how SL controls cell elongation via D53 and offer potential strategies to improve cotton quality through SL application.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"20 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887878","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":"HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis","authors":"Xiang Peng, Bin Sun, Chaohui Tang, Chengyu Shi, Xianwei Xie, Xueyu Wang, Dingsheng Jiang, Shuo Li, Ying Jia, Yani Wang, Huifang Tang, Shan Zhong, Minghui Piao, Xiuru Cui, Shenghao Zhang, Fan Wang, Yan Wang, Ruisi Na, Renping Huang, Yanan Jiang, Jinwei Tian","doi":"10.1016/j.devcel.2024.12.011","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.011","url":null,"abstract":"Advanced atherosclerosis is the pathological basis for acute cardiovascular events, with significant residual risk of recurrent clinical events despite contemporary treatment. The death of foamy macrophages is a main contributor to plaque progression, but the underlying mechanisms remain unclear. Bulk and single-cell RNA sequencing demonstrated that massive iron accumulation in advanced atherosclerosis promoted foamy macrophage ferroptosis, particularly in low expression of triggering receptor expressed on myeloid cells 2 (TREM2<sup>low</sup>) foamy macrophages. This cluster exhibits metabolic characteristics with low oxidative phosphorylation (OXPHOS), increasing ferroptosis sensitivity. Mechanically, upregulated heme oxygenase 1 (HMOX1)-lactate dehydrogenase B (LDHB) interaction enables Lon peptidase 1 (LONP1) to degrade mitochondrial transcription factor A (TFAM), leading to mitochondrial dysfunction and ferroptosis. Administration of the mitochondria-targeted reactive oxygen species (ROS) scavenger MitoTEMPO (mitochondrial-targeted TEMPO) or LONP1 inhibitor bortezomib restored mitochondrial homeostasis in foamy macrophages and alleviated atherosclerosis. Collectively, our study elucidates the cellular and molecular mechanism of foamy macrophage ferroptosis, offering potential therapeutic strategies for advanced atherosclerosis.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"33 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887881","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 : 2024-12-27DOI: 10.1016/j.devcel.2024.12.010
Pin-Ji Lei, Katarina J. Ruscic, Kangsan Roh, Johanna J. Rajotte, Meghan J. O’Melia, Echoe M. Bouta, Marla Marquez, Ethel R. Pereira, Ashwin S. Kumar, Mohammad S. Razavi, Hengbo Zhou, Lutz Menzel, Liqing Huang, Heena Kumra, Mark Duquette, Peigen Huang, James W. Baish, Lance L. Munn, Natasza A. Kurpios, Jessalyn M. Ubellacker, Timothy P. Padera
{"title":"Aging-induced changes in lymphatic muscle cell transcriptomes are associated with reduced pumping of peripheral collecting lymphatic vessels in mice","authors":"Pin-Ji Lei, Katarina J. Ruscic, Kangsan Roh, Johanna J. Rajotte, Meghan J. O’Melia, Echoe M. Bouta, Marla Marquez, Ethel R. Pereira, Ashwin S. Kumar, Mohammad S. Razavi, Hengbo Zhou, Lutz Menzel, Liqing Huang, Heena Kumra, Mark Duquette, Peigen Huang, James W. Baish, Lance L. Munn, Natasza A. Kurpios, Jessalyn M. Ubellacker, Timothy P. Padera","doi":"10.1016/j.devcel.2024.12.010","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.010","url":null,"abstract":"Lymphatic muscle cells (LMCs) within the wall of collecting lymphatic vessels exhibit tonic and autonomous phasic contractions, which drive active lymph transport to maintain tissue-fluid homeostasis and support immune surveillance. Damage to LMCs disrupts lymphatic function and is related to various diseases. Despite their importance, knowledge of the gene transcriptional signatures in LMCs and how they relate to lymphatic function in normal and disease contexts is largely missing. We have generated a comprehensive transcriptional single-cell atlas—including LMCs—of peripheral collecting lymphatic vessels from mice across the lifespan. We identified genes that distinguish LMCs from other types of muscle cells, characterized the phenotypical and transcriptomic changes in LMCs in aged vessels, and identified a proinflammatory microenvironment that suppresses the contractile apparatus in LMCs from advanced-aged mice. Our findings provide a valuable resource to accelerate future research for the identification of potential drug targets on LMCs to improve lymphatic vessel function.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"313 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887879","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":"Nucleolar protein PEXF controls ribosomal RNA synthesis and pluripotency exit","authors":"Zihao Li, Siwen Chen, Sifang Li, Hua Chao, Wenjun Hao, Shuai Zhang, Zemin Li, Jianru Wang, Xiang Li, Yong Wan, Hui Liu","doi":"10.1016/j.devcel.2024.12.004","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.004","url":null,"abstract":"Maintenance and exit from pluripotency of embryonic stem cells (ESCs) are controlled by highly coordinated processes of protein synthesis and ribosome biogenesis (RiBi). ESCs are characterized by low rates of global protein synthesis and high levels of RiBi. Transient reduction of RiBi is a characteristic molecular event during the exit from pluripotency, of which the regulatory mechanism is unclear. Here, we identify that a previously uncharacterized nucleolar protein, pluripotency exit factor (PEXF), encoded by long noncoding RNA <em>LINC00472</em>, plays a role in the transient reduction of RiBi. PEXF dissociates RNA polymerase I from the rDNA through interaction with the rDNA promoter region in a liquid-liquid phase separation-dependent manner, therefore inhibiting the production of pre-ribosomal RNA, a key component of ribosomes. This finding reveals a potential mechanism of exit from pluripotency gated by ribosome levels in human ESCs.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"41 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886696","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 : 2024-12-26DOI: 10.1016/j.devcel.2024.12.005
David Remy, Sandra Antoine-Bally, Sophie de Toqueville, Célia Jolly, Anne-Sophie Macé, Gabriel Champenois, Fariba Nemati, Isabel Brito, Virginie Raynal, Amulya Priya, Adèle Berlioz, Ahmed Dahmani, André Nicolas, Didier Meseure, Elisabetta Marangoni, Philippe Chavrier
{"title":"TFEB triggers a matrix degradation and invasion program in triple-negative breast cancer cells upon mTORC1 repression","authors":"David Remy, Sandra Antoine-Bally, Sophie de Toqueville, Célia Jolly, Anne-Sophie Macé, Gabriel Champenois, Fariba Nemati, Isabel Brito, Virginie Raynal, Amulya Priya, Adèle Berlioz, Ahmed Dahmani, André Nicolas, Didier Meseure, Elisabetta Marangoni, Philippe Chavrier","doi":"10.1016/j.devcel.2024.12.005","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.005","url":null,"abstract":"The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is frequently hyperactivated in triple-negative breast cancers (TNBCs) associated with poor prognosis and is a therapeutic target in breast cancer management. Here, we describe the effects of repression of mTOR-containing complex 1 (mTORC1) through knockdown of several key mTORC1 components or with mTOR inhibitors used in cancer therapy. mTORC1 repression results in an ∼10-fold increase in extracellular matrix proteolytic degradation. Repression in several TNBC models, including in patient-derived xenografts (PDXs), induces nuclear translocation of transcription factor EB (TFEB), which drives a transcriptional program that controls endolysosome function and exocytosis. This response triggers a surge in endolysosomal recycling and the surface exposure of membrane type 1 matrix metalloproteinase (MT1-MMP) associated with invadopodia hyperfunctionality. Furthermore, repression of mTORC1 results in a basal-like breast cancer cell phenotype and disruption of ductal carcinoma <em>in situ</em> (DCIS)-like organization in a tumor xenograft model. Altogether, our data call for revaluation of mTOR inhibitors in breast cancer therapy.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"31 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887055","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 : 2024-12-26DOI: 10.1016/j.devcel.2024.11.022
Vidur Garg, Yang Yang, Sonja Nowotschin, Manu Setty, Eralda Salataj, Ying-Yi Kuo, Dylan Murphy, Roshan Sharma, Amy Jang, Alexander Polyzos, Dana Pe’er, Effie Apostolou, Anna-Katerina Hadjantonakis
{"title":"Single-cell analysis of bidirectional reprogramming between early embryonic states identify mechanisms of differential lineage plasticities in mice","authors":"Vidur Garg, Yang Yang, Sonja Nowotschin, Manu Setty, Eralda Salataj, Ying-Yi Kuo, Dylan Murphy, Roshan Sharma, Amy Jang, Alexander Polyzos, Dana Pe’er, Effie Apostolou, Anna-Katerina Hadjantonakis","doi":"10.1016/j.devcel.2024.11.022","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.11.022","url":null,"abstract":"Two distinct lineages, pluripotent epiblast (EPI) and primitive (extra-embryonic) endoderm (PrE), arise from common inner cell mass (ICM) progenitors in mammalian embryos. To study how these sister identities are forged, we leveraged mouse embryonic stem (ES) cells and extra-embryonic endoderm (XEN) stem cells—<em>in vitro</em> counterparts of the EPI and PrE. Bidirectional reprogramming between ES and XEN coupled with single-cell RNA and ATAC-seq analyses showed distinct rates, efficiencies, and trajectories of state conversions, identifying drivers and roadblocks of reciprocal conversions. While GATA4-mediated ES-to-iXEN conversion was rapid and nearly deterministic, OCT4-, KLF4-, and SOX2-induced XEN-to-induced pluripotent stem (iPS) reprogramming progressed with diminished efficiency and kinetics. A dominant PrE transcriptional program, safeguarded by GATA4, alongside elevated chromatin accessibility and reduced DNA methylation of the EPI underscored the differential plasticities of the two states. Mapping <em>in vitro</em> to embryo trajectories tracked reprogramming cells in either direction along EPI and PrE <em>in vivo</em> states, without transitioning through the ICM.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"1 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886697","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":"Natural variation in an HD-ZIP factor identifies its role in controlling apple leaf cuticular wax deposition","authors":"Fuguo Cao, Qian Qian, Zhongxing Li, Jingrong Wang, Zeyuan Liu, Zitong Zhang, Chundong Niu, Yinpeng Xie, Fengwang Ma, Qingmei Guan","doi":"10.1016/j.devcel.2024.12.001","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.001","url":null,"abstract":"Natural variation is an invaluable genetic resource for plant trait improvement. Here, we performed a genome-wide association study (GWAS) analysis and identified MdHDG5, which controls apple leaf cuticular wax. An A-to-G single-nucleotide polymorphism (SNP) on the <em>HDG5</em> promoter is associated with <em>HDG5</em> expression and hexacosanol content (a component of leaf cuticular wax). Furthermore, the single-nucleotide variation (G/G) within a MYB <em>cis</em>-regulatory element (CRE) can be directly bound by MYB62, which represses <em>HDG5</em> expression and leaf wax deposition. In addition, MdPIAL2, a Small Ubiquitin-like Modifier (SUMO) E3 ligase, positively controls apple leaf wax deposition by stabilizing MdHDG5, while MdMIEL1 interacts with and degrades both MdHDG5 and MdPIAL2 to negatively control leaf wax deposition. Notably, <em>MIEL1</em> expression is negatively associated with leaf hexacosanol deposition. Taken together, our results provide significant genetic insights into the natural variation of leaf cuticular wax loads in apple and identify the intricate molecular regulation of MdHDG5.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"113 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880112","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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