{"title":"The complete reference genome of Tartary buckwheat and its mutation library provide important resources for genetic studies and breeding.","authors":"Hongyou Li, Qiuyu Lv, Taoxiong Shi, Yaling Jian, Bin Ran, Yuanzhi Cheng, Lei Wang, Jing Zhang, Juan Huang, Jiao Deng, Liwei Zhu, Qijiao Chen, Fang Cai, Ruiyuan Li, Qi Wu, Yizhong Zhang, Yuliang Zhang, Zhang Zhang, Feng Yu, Qingfu Chen","doi":"10.1016/j.celrep.2025.115621","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115621","url":null,"abstract":"<p><p>Tartary buckwheat (TB), Fagopyrum tataricum, is an important medicinal and edible crop with a worldwide distribution. However, reference genomes with gaps and mutant population scarcity have hindered functional genomics and genetic improvement of TB. Here, we present a telomere-to-telomere (T2T) gap-free genome assembly of the elite TB inbred line Guiku1 and its ethyl-methyl-sulfonate (EMS)-induced phenotypically rich mutation library. The Guiku1 gap-free genome spans 453.83 Mb, containing 43,441 predicted protein-coding genes. The mutation library includes 751 mutants with stably heritable phenotypes. Whole-genome resequencing of 320 mutants identified 105,682 single-nucleotide polymorphisms (SNPs) and 21,461 insertions/deletions (indels), affecting the protein-coding sequences of 25,986 genes. Genes responsible for the pink stem and petiole mutant trait and flavonoid content variation were identified using forward- and reverse-genetics approaches, respectively. Collectively, the T2T gap-free genome of Guiku1 and its EMS mutation library provide important resources for functional genomics studies and the genetic improvement of TB.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115621"},"PeriodicalIF":7.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987104","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}
Cell reportsPub Date : 2025-05-05DOI: 10.1016/j.celrep.2025.115648
Cheng-Yen Chen, Naweed I Naqvi
{"title":"Endophytic mycobiont provides growth benefits via a phenylpropanoid-auxin axis in host plants.","authors":"Cheng-Yen Chen, Naweed I Naqvi","doi":"10.1016/j.celrep.2025.115648","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115648","url":null,"abstract":"<p><p>Beneficial association with symbiotic fungi helps improve growth and fitness in most land plants and shows great potential as biofertilizers in precision agriculture. Here, we demonstrated that a root fungal endophyte, Tinctoporellus species isolate AR8, enabled yield improvement in Brassicaceae leafy green choy sum (Brassica rapa var. parachinensis). Mechanistically, AR8 colonized the root cortex/endosphere and channeled the metabolic flux to phenylpropanoids and requisite secondary metabolites to promote plant growth. AR8-assisted biosynthesis of auxin improved root growth and provided an intrinsic source for long-distance signaling that enhanced shoot biomass. Chemical complementation with exogenous p-coumaric acid restored auxin signaling and enhanced growth in AR8-inoculated pal1 mutant plants, thus implicating such a phenylpropanoid-auxin nexus as a pivotal regulator of symbiotic plant growth. Comparative metabolomics established hydroxycinnamic acid and p-coumaric acid as major plant-growth-promoting hubs that bridge the phenylpropanoid pathway and auxin signaling in the cross-kingdom AR8 symbiotic interaction model.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115648"},"PeriodicalIF":7.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975250","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}
Cell reportsPub Date : 2025-05-05DOI: 10.1016/j.celrep.2025.115652
Andrea Gramatica, Itzayana G Miller, Adam R Ward, Farzana Khan, Tyler J Kemmer, Jared Weiler, Tan Thinh Huynh, Paul Zumbo, Andrew P Kurland, Louise Leyre, Yanqin Ren, Thais Klevorn, Dennis C Copertino, Uchenna Chukwukere, Callie Levinger, Thomas R Dilling, Noemi Linden, Nathan L Board, Emma Falling Iversen, Sandra Terry, Talia M Mota, Seden Bedir, Kiera L Clayton, Alberto Bosque, Lynsay MacLaren Ehui, Colin Kovacs, Doron Betel, Jeffry R Johnson, Mirko Paiardini, Ali Danesh, R Brad Jones
{"title":"EZH2 inhibition mitigates HIV immune evasion, reduces reservoir formation, and promotes skewing of CD8<sup>+</sup> T cells toward less-exhausted phenotypes.","authors":"Andrea Gramatica, Itzayana G Miller, Adam R Ward, Farzana Khan, Tyler J Kemmer, Jared Weiler, Tan Thinh Huynh, Paul Zumbo, Andrew P Kurland, Louise Leyre, Yanqin Ren, Thais Klevorn, Dennis C Copertino, Uchenna Chukwukere, Callie Levinger, Thomas R Dilling, Noemi Linden, Nathan L Board, Emma Falling Iversen, Sandra Terry, Talia M Mota, Seden Bedir, Kiera L Clayton, Alberto Bosque, Lynsay MacLaren Ehui, Colin Kovacs, Doron Betel, Jeffry R Johnson, Mirko Paiardini, Ali Danesh, R Brad Jones","doi":"10.1016/j.celrep.2025.115652","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115652","url":null,"abstract":"<p><p>Persistent HIV reservoirs in CD4<sup>+</sup> T cells pose a barrier to curing HIV infection. We identify overexpression of enhancer of zeste homolog 2 (EZH2) in HIV-infected CD4<sup>+</sup> T cells that survive cytotoxic T lymphocyte (CTL) exposure, suggesting a mechanism of CTL resistance. Inhibition of EZH2 with the US Food and Drug Administration-approved drug tazemetostat increases surface expression of major histocompatibility complex (MHC) class I on CD4<sup>+</sup> T cells, counterbalancing HIV Nef-mediated MHC class I downregulation. This improves CTL-mediated elimination of HIV-infected cells and suppresses viral replication in vitro. In a participant-derived xenograft mouse model, tazemetostat elevates MHC class I and the pro-apoptotic protein BIM in CD4<sup>+</sup> T cells, facilitating CD8<sup>+</sup> T cell-mediated reductions of HIV reservoir seeding. Additionally, tazemetostat promotes sustained skewing of CD8<sup>+</sup> T cells toward less-differentiated and exhausted phenotypes. Our findings reveal EZH2 overexpression as a mechanism of CTL resistance and support the clinical evaluation of tazemetostat as a method of enhancing clearance of HIV reservoirs and improving CD8<sup>+</sup> T cell function.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115652"},"PeriodicalIF":7.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986074","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}
Cell reportsPub Date : 2025-05-05DOI: 10.1016/j.celrep.2025.115641
Fanlong Wang, Mingliang Qiu, Lei Hou, Xianbi Li, Hui Ren, Jingxin Zhuo, Haoru Liu, Yujie Li, Yang Yang, Xingying Yan, Mi Zhang, Dan Jin, Ting Lan, Jianyan Zeng, Yanhua Fan, Yang Yuan, Zhengqiang Ma, Yan Pei
{"title":"N terminus and C terminus of Arabidopsis P4-ATPase AtALA1 facilitate the detoxification of the mycotoxin deoxynivalenol in wheat.","authors":"Fanlong Wang, Mingliang Qiu, Lei Hou, Xianbi Li, Hui Ren, Jingxin Zhuo, Haoru Liu, Yujie Li, Yang Yang, Xingying Yan, Mi Zhang, Dan Jin, Ting Lan, Jianyan Zeng, Yanhua Fan, Yang Yuan, Zhengqiang Ma, Yan Pei","doi":"10.1016/j.celrep.2025.115641","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115641","url":null,"abstract":"<p><p>Fusarium head blight (FHB) is a devastating disease affecting many important cereal crops. The disease is mainly caused by Fusarium graminearum, which produces mycotoxins, e.g., deoxynivalenol (DON), that contaminate grains, leading to serious issues in food safety worldwide. Here, we demonstrate that expressing the Arabidopsis P4-ATPase flippase gene, AtALA1, significantly increases wheat resistance to FHB, while substantially reducing DON content in grains. However, expressing TaALA1s, the wheat homologs of AtALA1, does not enhance the resistance. We discovered that the N terminus and C terminus of AtALA1 are crucial for its role in DON detoxification. The motif [DE]<sub>n</sub>X<sub>1-2</sub>FXX[FL]XXXR, found exclusively in the N terminus of ALA1s in Brassicaceae species, facilitates AtALA1-associated vesicle transport by binding with AP-2. Meanwhile the DON-stimulated phosphorylation at three key sites in the C terminus is responsible for promoting DON trafficking into vacuoles. Our findings suggest a great potential for vesicle-associated detoxification in FHB resistance and food safety.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115641"},"PeriodicalIF":7.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978784","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}
Cell reportsPub Date : 2025-05-05DOI: 10.1016/j.celrep.2025.115644
Landen Gozashti, Olivia S Harringmeyer, Hopi E Hoekstra
{"title":"How repeats rearrange chromosomes: The molecular basis of chromosomal inversions in deer mice.","authors":"Landen Gozashti, Olivia S Harringmeyer, Hopi E Hoekstra","doi":"10.1016/j.celrep.2025.115644","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115644","url":null,"abstract":"<p><p>Large genomic rearrangements, such as chromosomal inversions, can play a key role in evolution, but the mechanisms by which these rearrangements arise remain poorly understood. To study the origins of inversions, we generated chromosome-level de novo genome assemblies for four subspecies of the deer mouse (Peromyscus maniculatus) with known inversion polymorphisms. We identified ∼8,000 inversions, including 47 megabase-scale inversions, that together affect ∼30% of the genome. Analysis of inversion breakpoints suggests that while most small (<1 Mb) inversions arose via ectopic recombination between retrotransposons, large (>1 Mb) inversions are primarily associated with segmental duplications (SDs). Large inversion breakpoints frequently occur near centromeres, which may be explained by an accumulation of retrotransposons in pericentromeric regions driving SDs. Additionally, multiple large inversions likely arose from ectopic recombination between near-identical centromeric satellite arrays located megabases apart, suggesting that centromeric repeats may also facilitate inversions. Together, our results illuminate how repeats give rise to massive shifts in chromosome architecture.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115644"},"PeriodicalIF":7.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981561","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}
Cell reportsPub Date : 2025-05-03DOI: 10.1016/j.celrep.2025.115654
Francisco E Neal, Wenjing Li, Mollie E Uhrig, Jeffrey N Katz, Shahrez Syed, Neelam Sharma, Arijit Dutta, Sandeep Burma, Robert Hromas, Alexander V Mazin, Eloise Dray, David S Libich, Shaun K Olsen, Elizabeth V Wasmuth, Weixing Zhao, Claus S Sørensen, Claudia Wiese, Youngho Kwon, Patrick Sung
{"title":"Distinct roles of the two BRCA2 DNA-binding domains in DNA damage repair and replication fork preservation.","authors":"Francisco E Neal, Wenjing Li, Mollie E Uhrig, Jeffrey N Katz, Shahrez Syed, Neelam Sharma, Arijit Dutta, Sandeep Burma, Robert Hromas, Alexander V Mazin, Eloise Dray, David S Libich, Shaun K Olsen, Elizabeth V Wasmuth, Weixing Zhao, Claus S Sørensen, Claudia Wiese, Youngho Kwon, Patrick Sung","doi":"10.1016/j.celrep.2025.115654","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115654","url":null,"abstract":"<p><p>Homologous recombination (HR) removes DNA double-strand breaks (DSBs) and preserves stressed DNA replication forks. Successful HR execution requires the tumor suppressor BRCA2, which harbors distinct DNA-binding domains (DBDs): one that possesses three oligonucleotide/oligosaccharide-binding (OB) folds (OB-DBD) and another residing in the C-terminal recombinase binding domain (CTRB-DBD). Here, we employ multi-faceted approaches to delineate the contributions of these domains toward HR and replication fork maintenance. We show that OB-DBD and CTRB-DBD confer single-strand DNA (ssDNA)- and dsDNA-binding capabilities, respectively, and that BRCA2 variants mutated in either domain are impaired in their ability to load the recombinase RAD51 onto ssDNA pre-occupied by RPA. While the CTRB-DBD mutant is modestly affected by DNA break repair, it exhibits a strong defect in the protection of stressed replication forks. In contrast, the OB-DBD is indispensable for both BRCA2 functions. Our study thus defines the unique contributions of the two BRCA2 DBDs in genome maintenance.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115654"},"PeriodicalIF":7.5,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965736","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":"RABC1-ABI1 module coordinates lipid droplet mobilization and post-germination growth arrest in Arabidopsis.","authors":"Yifei Wang, Min Zhang, Pengyue Sun, Xin Zhao, Ruo-Xi Zhang, Yun-Kuan Liang","doi":"10.1016/j.celrep.2025.115655","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115655","url":null,"abstract":"<p><p>Abscisic acid (ABA) promotes post-germination growth arrest (PGGA), thereby enhancing plant survival under adverse conditions such as high salinity. Lipid droplets (LDs) are universally conserved dynamic organelles that can store and mobilize neutral lipids for their multiple cellular roles. The molecular mechanism whereby a plant coordinates LD mobilization and PGGA in response to environmental stresses remains poorly understood. Here, we report that RABC1 deficiency enhances PGGA, which could be efficiently mitigated by either inhibiting ABA biosynthesis or promoting LD breakdown. ABI1 interacts with and dephosphorylates RABC1 and promotes the interactions between RABC1 and its effectors SEIPIN2 and SEIPIN3, consequently enhancing LD mobilization. Taken together, these results report a regulatory mechanism of LD mobilization for plant stress tolerance and highlight a concerted interplay between lipid metabolism and hormonal signaling.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115655"},"PeriodicalIF":7.5,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966224","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":"ER-PM tether Syt1 limits cell-to-cell connectivity via plasmodesmata during innate immune responses in Arabidopsis.","authors":"Jiajing Li, Pengfei Lu, Qing Pan, Bingxiao Wang, Youjun Wang, Jiejie Li","doi":"10.1016/j.celrep.2025.115672","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115672","url":null,"abstract":"<p><p>Upon perception of microbe-associated molecular patterns (MAMPs), plants close plasmodesmata (PD) as part of their innate immune responses. However, the signaling cascades and molecular mechanisms underlying MAMP-induced PD closure require further investigation. Here, we show that the endoplasmic reticulum (ER)-plasma membrane (PM) tether Synaptotagmin 1 (Syt1) modulates the response of PD to MAMPs. Following MAMP stimulation, Syt1 rapidly accumulates to PD and further recruits a putative calcium-permeable transporter, ANN4, to promote a localized, PD-associated Ca<sup>2+</sup> elevation, leading to callose-dependent PD closure. Moreover, Syt1 can sense the increased level of PI(4,5)P<sub>2</sub> at the PD-PM via its C2 domain. Disrupting the interaction between Syt1 and PM lipids by pharmaceutical approaches or site-directed mutagenesis leads to impaired PD response to MAMPs. Collectively, our findings reveal that Syt1 integrates phospholipid signaling from the PD-PM to regulate PD-localized Ca<sup>2+</sup> elevation, thereby modulating intercellular communication for restricting the spread of bacterial infection.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115672"},"PeriodicalIF":7.5,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978596","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}
Cell reportsPub Date : 2025-05-03DOI: 10.1016/j.celrep.2025.115653
Karl Kuchler
{"title":"Hepcidin and fungal infections: The liver fights back.","authors":"Karl Kuchler","doi":"10.1016/j.celrep.2025.115653","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115653","url":null,"abstract":"<p><p>Arekar et al. demonstrate that the liver peptide hepcidin holds therapeutic promises for treating invasive fungal infections by Candida albicans.<sup>1</sup> A hepcidin agonist improves infection outcome because it protects from renal pathology by diminishing iron bioavailability in kidneys.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115653"},"PeriodicalIF":7.5,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966138","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}
Cell reportsPub Date : 2025-05-02DOI: 10.1016/j.celrep.2025.115659
Linghui Pan, Ruihua Li, Qiqi Li, Qin Zhu, Qian Zhou, Aru Su, Renli Qi, Zuohua Liu, Ruifan Wu, Songbo Wang, Lina Wang, Gang Shu, Qingyan Jiang, Canjun Zhu
{"title":"The gut-brain axis mechanism of normal appetite induced by kynurenic acid.","authors":"Linghui Pan, Ruihua Li, Qiqi Li, Qin Zhu, Qian Zhou, Aru Su, Renli Qi, Zuohua Liu, Ruifan Wu, Songbo Wang, Lina Wang, Gang Shu, Qingyan Jiang, Canjun Zhu","doi":"10.1016/j.celrep.2025.115659","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.115659","url":null,"abstract":"<p><p>Feeding is essential for both host-organism survival and gut-microbiota maintenance. Our research focuses on how kynurenic acid (KYNA), a gut-microbiota metabolite, regulates appetite during fasting. We find that fasting significantly raises KYNA levels in the intestine, which increases short-term food intake by inhibiting vagal afferent nerve in the nodose ganglion (NG) and activating AgRP neurons in arcuate nucleus (ARC<sup>AgRP</sup>). The orexigenic effects of KYNA are abolished by subdiaphragmatic vagotomy (sdVx), chemogenetic activation/inhibition of glutamatergic NG/ARC<sup>AgRP</sup> neurons, inhibiting the nucleus of the solitary tract (NTS) to ARC<sup>AgRP</sup> inputs, or knockdown of GPR35 (a KYNA receptor) in the intestinal vagal afferent nerve. Our data support a model in which KYNA acts through the GPR35 receptor to inhibit vagal afferent signaling and subsequently activate ARC<sup>AgRP</sup> neurons, which leads to increased food intake. These findings reveal a mechanism by which gut microbiota controls appetite during fasting, highlighting the complex relationship between microbial and host feeding behavior.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 5","pages":"115659"},"PeriodicalIF":7.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978239","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}