PLoS Genetics最新文献

{"title":"Correction: Functional redundancy and formin-isoform independent localization of tropomyosin paralogs in Saccharomyces cerevisiae.","authors":"","doi":"10.1371/journal.pgen.1012065","DOIUrl":"https://doi.org/10.1371/journal.pgen.1012065","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1371/journal.pgen.1011859.].</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012065"},"PeriodicalIF":3.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Rad54 separation of function mutation highlights unique roles during homologous recombination.","authors":"Jingyi Hu, David Moraga, Amanda Xu, Lauren Peysakhova, J Brooks Crickard","doi":"10.1371/journal.pgen.1012136","DOIUrl":"10.1371/journal.pgen.1012136","url":null,"abstract":"<p><p>Homologous recombination (HR) is a DNA repair pathway that utilizes a template-based approach to repair double-strand breaks within the genome. Template use requires the exchange of individual DNA strands, which members of the RecA family of recombinases facilitate. Rad51 is a primary strand exchange factor in eukaryotes. During regular mitotic DNA repair, Rad51 is aided by the DNA translocase Rad54, which acts as a motor to remodel the template DNA and stabilize primary-strand exchange intermediates. The regulation of this activity remains incompletely understood. Here, we have identified a conserved site within the C-terminal region of Rad54. The mutation of this site creates a separation of function at early strand-exchange intermediates in vivo. Using this mutant protein, we identify a novel intermediate essential for stabilizing displacement loop (D-loop) structures. This precedes the removal of Rad51 and DNA extension. Based on our experiments, we hypothesize that this Rad54 mutant cannot stabilize Rad51-mediated strand-exchange intermediates due to slippage during translocation, leading to failure in DNA remodeling. Identifying a mutant that disrupts this intermediate before Rad51 removal unifies existing models of Rad54-mediated D-loop formation and extension.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012136"},"PeriodicalIF":3.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13138755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pos-1 3' untranslated region governs germline specification and proliferation to ensure reproductive robustness.","authors":"Haik V Varderesian, Juliet N Utaegbulam, Hannah E Brown, Beverly Ramirez, Melina Velcani, Sean P Ryder","doi":"10.1371/journal.pgen.1012129","DOIUrl":"10.1371/journal.pgen.1012129","url":null,"abstract":"<p><p>During fertilization, haploid gametes combine to form a zygote. The male (sperm) and female (oocyte) gametes contribute a similar amount of DNA, but the oocyte contributes nearly all the cytoplasm. Oocytes are loaded with maternal mRNAs thought to be essential for embryonic patterning after fertilization. A conserved suite of RNA-binding proteins (RBPs) regulates the spatiotemporal translation and stability of maternal mRNAs. POS-1 is a CCCH-type tandem zinc finger RBP expressed in fertilized Caenorhabditis elegans zygotes from maternally supplied mRNA. POS-1 accumulates in the posterior of the embryo where it promotes posterior cell fate. Here, we show that the pos-1 3' untranslated region (UTR) is essential for POS-1 patterning and contributes to maximal reproductive fecundity. We engineered a pos-1 mutant where most of the endogenous pos-1 3'UTR was removed using CRISPR genome editing. Our results show that the 3'UTR represses POS-1 expression in the maternal germline but increases POS-1 protein levels in embryos after fertilization. In a wild-type background, POS-1 repression via the 3'UTR has little impact on fertility. In a sensitized background, the deletion mutant has a complex pleiotropic phenotype where most adult homozygous progeny lack either one or both gonad arms. Most phenotypes become more penetrant at elevated temperature. Together, our results support an emerging model where the 3'UTRs of maternal transcripts, rather than being essential, contribute to reproductive robustness during stress.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012129"},"PeriodicalIF":3.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nebivolol suppresses glioblastoma progression via dual modulation of mitochondrial metabolism and AKT/mTOR/4EBP1 signaling axis.","authors":"Lingni Zhou, Hongyu Che, Hongyan Jiang, Luxin Yin, Yongang Jiang, Yuhui Zhang, Haoran Liang, Rutong Yu, Xu Zhang, Xuejiao Liu","doi":"10.1371/journal.pgen.1012120","DOIUrl":"https://doi.org/10.1371/journal.pgen.1012120","url":null,"abstract":"<p><p>Emerging evidence reveals the pivotal involvement of mitochondrial metabolic dysregulation in glioblastoma (GBM) pathogenesis, considering mitochondrial metabolism as a potential therapeutic target. Nebivolol, a third-generation β-adrenergic receptor antagonist clinically employed in cardiovascular diseases, has recently exhibited notable anti-neoplastic properties. Nevertheless, its therapeutic efficacy and mechanistic underpinnings in GBM remain largely unexplored. In this investigation, we comprehensively assessed the impact of nebivolol on GBM cellular proliferation and elucidated its molecular mechanisms. Our findings revealed that nebivolol markedly suppressed the proliferation and clonogenic abilities of multiple GBM cell lines, concomitant with cell cycle arrest and apoptotic induction. Mechanistically, nebivolol impaired mitochondrial respiratory chain complex I activity, diminished adenosine triphosphate (ATP) synthesis, and augmented ROS production, collectively precipitating neoplastic cell apoptosis. Furthermore, nebivolol attenuated AKT/mTOR/4EBP1 signaling cascade activation, thereby impeding GBM malignant proliferation. In vivo studies corroborated these observations, demonstrating that nebivolol administration significantly attenuated orthotopic GBM xenograft progression and extended survival in tumor-bearing murine models. This study delineates a novel dual mechanism whereby nebivolol exerts anti-GBM effects through concurrent modulation of mitochondrial bioenergetics and AKT/mTOR/4EBP1 signaling transduction. These results provide robust preclinical evidence supporting nebivolol's clinical repurposing for GBM therapy.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012120"},"PeriodicalIF":3.7,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The transcription factor TaWRKY58 coordinates growth and drought sensitivity in wheat by repressing TaLRR and TaBCS1.","authors":"Yazhou Zhang, Xinyao Cheng, Xinyu Yu, Anyu Gu, Xufei Zhao, Mei Deng, Guoyue Cheng, Qiang Xu, Qiantao Jiang, Yuming Wei","doi":"10.1371/journal.pgen.1012124","DOIUrl":"10.1371/journal.pgen.1012124","url":null,"abstract":"<p><p>Balancing growth and stress adaptation is essential for optimizing crop productivity, yet the transcriptional mechanisms underlying this trade-off in wheat remain poorly understood. Here, we identify the WRKY transcription factor TaWRKY58 as a key repressor coordinating plant architecture and drought response. Loss-of-function mutants of TaWRKY58 exhibit increased plant height and early flowering, accompanied by elevated gibberellin levels, while overexpression restores wild-type phenotypes. Under drought stress, TaWRKY58 represses soluble sugar accumulation, and its mutants show enhanced drought tolerance. Using DAP-seq, we identified genome-wide binding sites of TaWRKY58 and uncovered a W-box-like motif enriched in its target promoters. Electrophoretic mobility shift and dual-luciferase assays confirmed that TaWRKY58 directly binds to and represses two key targets: TaLRR, encoding a leucine-rich repeat protein, and TaBCS1, encoding a mitochondrial AAA⁺ ATPase. Mutants of TaLRR and TaBCS1 display dwarfism and drought hypersensitivity, respectively, mirroring aspects of the TaWRKY58 overexpression phenotype. Our data support a model in which TaWRKY58 functions as a transcriptional repressor in a coherent regulatory module that fine-tunes growth and stress adaptation by modulating signaling and energy metabolism. This mechanism offers a potential strategy for breeding wheat with optimized yield stability under fluctuating environments.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012124"},"PeriodicalIF":3.7,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Regulatory rewiring drives intraspecies competition in Bacillus subtilis.","authors":"Margarita Kalamara, Alistair Bonsall, Jonathan Griffin, Joana Carneiro, Marek Gierlinski, Lukas Eigentler, David Stevenson, Amy Wood, Michael Porter, Helge C Dorfmueller, Cait E MacPhee, James C Abbott, Nicola R Stanley-Wall","doi":"10.1371/journal.pgen.1012128","DOIUrl":"https://doi.org/10.1371/journal.pgen.1012128","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1371/journal.pgen.1012050.].</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012128"},"PeriodicalIF":3.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic gene regulation is controlled by distinct regulatory complexes utilizing specialized paralogs of TELOMERE REPEAT BINDING FACTORS.","authors":"Maik Mendler, Kristin Krause, Simone Zündorf, Prathamesh Sannak, Petra Tänzler, Sara Stolze, Hirofumi Nakagami, Franziska Turck","doi":"10.1371/journal.pgen.1012114","DOIUrl":"10.1371/journal.pgen.1012114","url":null,"abstract":"<p><p>Epigenetic regulators shape chromatin landscapes, allowing cells to express distinct gene sets depending on cell-type, developmental stage or environmental cues. These regulatory complexes rely on interactions with sequence-specific DNA binding proteins, such as the small family of TELOMERE REPEAT BINDING FACTORS (TRBs). TRBs are components of chromatin regulatory complexes with opposing functions, such as the epigenetic repressors Polycomb Repressive Complex 2 (PRC2) and a JMJ14/NAC complex that respectively add and removes the repressive H3K27me3 and positive H3K4me3 modification, but also with the plant-specific PEAT complex that is linked to histone acetylation and gene activation. We dissected the partial redundancy between TRB1, TRB2 and TRB3 in target gene selection and interaction with different chromatin regulatory complexes. High redundancy of TRBs is suggested by major phenotypic changes that are only observed trb triple mutants; however, we found different target site preference between TRB1-3 and preferred partnership with chromatin complexes. Furthermore, TRB paralogs interacted with the NuA4 histone acetylation complex, both together with and in absence of PEAT. Among the three paralogs, TRB1 had more unique binding sites and correlated stronger with PEAT and NuA4 functions. In contrast, TRB2 and TRB3 were more dependent on the presence of bona fide telo-box motifs and were more likely to be found at PRC2 associated sites. Overall, we provide insight into the diverse roles of TRBs in epigenetic gene regulation and how their diversification contributes to their apparent redundancy, as well as their observed activating and repressing effects on gene expression.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012114"},"PeriodicalIF":3.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inducible gene deletion reveals essentiality of protein kinases and a septation initiation network in Candida albicans.","authors":"Bernardo Ramírez-Zavala, Ines Krüger, Sonja Schwanfelder, Johannes Lackner, Thomas Krüger, Olaf Kniemeyer, Joachim Morschhäuser","doi":"10.1371/journal.pgen.1012118","DOIUrl":"10.1371/journal.pgen.1012118","url":null,"abstract":"<p><p>Protein kinases are key components of many signaling pathways that regulate cellular activities, and some of them are indispensable for the viability of cells. We used inducible gene deletion to assess the importance of a set of putative essential protein kinases for growth and viability of the pathogenic yeast Candida albicans and to get clues about the functions of uncharacterized essential kinases. We found that bud32Δ, ctk1Δ, rio1Δ, and rio2Δ mutants were viable but grew very slowly, explaining previous failures to generate homozygous deletion mutants. PTK2 was essential, but under certain conditions ptk2Δ mutants remained viable and over time could acquire suppressor mutations in the Ptk2-dependent plasma membrane ATPase Pma1 that restored growth. Deletion of the uncharacterized orf19.5376 was lethal and the null mutants formed pseudohyphae that lacked normal septa and eventually lysed, a phenotype that was phenocopied by auxin-induced protein depletion. The mutants were defective in septin organization, indicating that the orf19.5376-encoded kinase is functionally similar to the nonessential kinase Elm1 of Saccharomyces cerevisiae, but is indispensable for viability in C. albicans. Mutants lacking orf19.3456, which does not have a homolog in S. cerevisiae, were also nonviable and grew as aseptate, sometimes multinucleate hyphae before cell death. Co-immunoprecipitation followed by liquid chromatography-mass spectrometry identified a protein, encoded by the uncharacterized orf19.193, as a candidate regulatory subunit of the orf19.3456-encoded kinase, as mutants lacking this protein exhibited the same terminal phenotype as orf19.3456 mutants. These results provide strong evidence that instead of using a mitotic exit network (MEN) with only two kinases (Cdc15 and Dbf2), as was previously thought, C. albicans regulates septum formation and cytokinesis via a septation initiation network (SIN), known from fission yeast and filamentous fungi, which contains a protein kinase cascade consisting of the upstream kinase Cdc15, the orf19.3456-encoded kinase, and the downstream kinase Dbf2.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012118"},"PeriodicalIF":3.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dominance modifiers at the Arabidopsis self-incompatibility locus retain proto-miRNA features and act through non-canonical pathways.","authors":"Rita A Batista, Eléonore Durand, Monika Mörchen, Jacinthe Azevedo-Favory, Samson Simon, Manu Dubin, Vinod Kumar, Eléanore Lacoste, Corinne Cruaud, Christelle Blassiau, Matteo Barois, Anne-Catherine Holl, Chloé Ponitzki, Nathalie Faure, William Marande, Sonia Vautrin, Isabelle Fobis-Loisy, Jean-Marc Aury, Sylvain Legrand, Ute Krämer, Thierry Lagrange, Xavier Vekemans, Vincent Castric","doi":"10.1371/journal.pgen.1012127","DOIUrl":"10.1371/journal.pgen.1012127","url":null,"abstract":"<p><p>Self-incompatibility in flowering plants is a common mechanism that prevents self-fertilization and promotes outcrossing. In Brassicaceae, the self-incompatibility locus is highly diverse, with many alleles arranged in a complex dominance hierarchy and exhibiting monoallelic expression in heterozygote individuals. Monoallelic expression of the pollen self-incompatibility gene is achieved through the action of sRNA precursors that resemble miRNAs, although the underlying molecular mechanisms remain elusive. Here, we engineered Arabidopsis thaliana lines expressing components of the Arabidopsis halleri self-incompatibility system, and used a reverse genetics approach to pinpoint the pathways underlying the function of these sRNA precursors. We showed that they trigger a robust decrease in transcript abundance of the recessive self-incompatibility genes, but not through the canonical transcriptional or post-transcriptional gene silencing pathways. Furthermore, we observed that single sRNA precursors are typically processed into hundreds of sRNA molecules with a variety of sizes, abundance levels and ARGONAUTE loading preferences. Our results suggest that these seemingly arbitrary processing characteristics are essential for establishing the self-incompatibility dominance hierarchy, as they enable a single sRNA precursor from a dominant allele to effectively repress multiple recessive alleles, thus providing a unique example of how small RNAs mediate gene silencing within a highly complex regulatory network.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012127"},"PeriodicalIF":3.7,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Examining the association between fetal HLA-C, maternal KIR haplotypes and birth weight.","authors":"Caitlin Stephanie Decina, Nicole M Warrington, Robin N Beaumont, Beilei Bian, Caroline Brito Nunes, Geng Wang, William L Lowe, David Squire, Damjan Vukcevic, Stephen Leslie, Rachel M Freathy, David M Evans","doi":"10.1371/journal.pgen.1012102","DOIUrl":"10.1371/journal.pgen.1012102","url":null,"abstract":"<p><p>Human birth weight is under stabilizing selection, seeking balance between extremes of high and low, thereby reducing fetal and maternal perinatal mortality risk. Certain combinations of maternal killer immunoglobulin-like receptor (KIR) and paternally derived fetal human leuokocyte antigen-C (HLA-C) alleles were previously associated with higher risk of high and low birth weight in a study with limited sample size (n = 1,316). Using recently developed methods to impute HLA and KIR haplotypes using single nucleotide polymorphism (SNP) genotype data, we tested associations of fetal HLA and maternal KIR genotypes with offspring birth weight in a large sample. We imputed KIR haplotypes using the KIR*IMP imputation software in 10,602 mother-offspring pairs of European descent from singleton pregnancies from five studies. Using mixed linear regression models to account for mothers with multiple children, we tested associations between maternal KIR A vs B haplotypes (AA, AB/BA, BB genotypes) as well as copy number of activating receptor gene KIR2DS1 (0, 1, 2 copies of the gene) in the presence of fetal HLA C1/C2 alleles, and offspring birth weight. Associations were analyzed in each cohort before performing a meta-analysis to estimate the interaction effects between maternal KIR and fetal HLA-C2 on birth weight across the entire sample. The KIR haplotypes achieved imputation accuracy estimated at >95% in most of the cohorts. No interaction effects were observed between either the maternal A vs. B haplotype or the maternal KIR2DS1 locus and fetal HLA-C. When specifically trying to replicate the previously associated combination of maternal KIR2DS1 and paternally inherited fetal HLA-C2, there was a negligible change in offspring birth weight for each additional KIR2DS1 allele and HLA-C2 of paternal origin (7g lower birth weight per allele [95% CI: -54, 40], P = 0.78). We found little evidence of association between birth weight and maternal KIR haplotypes or fetal HLA-C2 and were unable to replicate previously reported findings. Our observations reinforce the importance of replication and the use of large sample sizes in the validation of genetic associations.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 4","pages":"e1012102"},"PeriodicalIF":3.7,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13095029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}