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  • 1
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    LECT2, a Ligand for Tie1, Plays a Crucial Role in Liver Fibrogenesis (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 29 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell〈/p〉 〈p〉Author(s): Meng Xu, Hong-Hai Xu, Yuan Lin, Xiangnan Sun, Li-Jing Wang, Zhe-Ping Fang, Xue-Han Su, Xiang-Jing Liang, Yang Hu, Zhi-Min Liu, Yuanxiong Cheng, Yuanyuan Wei, Jiabin Li, Li Li, Hong-Juan Liu, Zhiqiang Cheng, Na Tang, Chao Peng, Tingting Li, Tengfei Liu〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Liver fibrosis is a very common condition seen in millions of patients with various liver diseases, and yet no effective treatments are available owing to poorly characterized molecular pathogenesis. Here, we show that leukocyte cell-derived chemotaxin 2 (LECT2) is a functional ligand of Tie1, a poorly characterized endothelial cell (EC)-specific orphan receptor. Upon binding to Tie1, LECT2 interrupts Tie1/Tie2 heterodimerization, facilitates Tie2/Tie2 homodimerization, activates PPAR signaling, and inhibits the migration and tube formations of EC. 〈em〉In vivo〈/em〉 studies showed that LECT2 overexpression inhibits portal angiogenesis, promotes sinusoid capillarization, and worsens fibrosis, whereas these changes were reversed in 〈em〉Lect2-KO〈/em〉 mice. Adeno-associated viral vector serotype 9 (AAV9)-LECT2 small hairpin RNA (shRNA) treatment significantly attenuates fibrosis. Upregulation of LECT2 is associated with advanced human liver fibrosis staging. We concluded that targeting LECT2/Tie1 signaling may represent a potential therapeutic target for liver fibrosis, and serum LECT2 level may be a potential biomarker for the screening and diagnosis of liver fibrosis.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S009286741930786X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 2
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    TNF Induces Pathogenic Programmed Macrophage Necrosis in Tuberculosis through a Mitochondrial-Lysosomal-Endoplasmic Reticulum Circuit (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 29 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell〈/p〉 〈p〉Author(s): Francisco J. Roca, Laura J. Whitworth, Sarah Redmond, Ana A. Jones, Lalita Ramakrishnan〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Necrosis of infected macrophages constitutes a critical pathogenetic event in tuberculosis by releasing mycobacteria into the growth-permissive extracellular environment. In zebrafish infected with 〈em〉Mycobacterium marinum〈/em〉 or 〈em〉Mycobacterium tuberculosis〈/em〉, excess tumor necrosis factor triggers programmed necrosis of infected macrophages through the production of mitochondrial reactive oxygen species (ROS) and the participation of cyclophilin D, a component of the mitochondrial permeability transition pore. Here, we show that this necrosis pathway is not mitochondrion-intrinsic but results from an inter-organellar circuit initiating and culminating in the mitochondrion. Mitochondrial ROS induce production of lysosomal ceramide that ultimately activates the cytosolic protein BAX. BAX promotes calcium flow from the endoplasmic reticulum into the mitochondrion through ryanodine receptors, and the resultant mitochondrial calcium overload triggers cyclophilin-D-mediated necrosis. We identify ryanodine receptors and plasma membrane L-type calcium channels as druggable targets to intercept mitochondrial calcium overload and necrosis of mycobacterium-infected zebrafish and human macrophages.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S009286741930892X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 3
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    A Structure-Informed Atlas of Human-Virus Interactions (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 29 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell〈/p〉 〈p〉Author(s): Gorka Lasso, Sandra V. Mayer, Evandro R. Winkelmann, Tim Chu, Oliver Elliot, Juan Angel Patino-Galindo, Kernyu Park, Raul Rabadan, Barry Honig, Sagi D. Shapira〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉While knowledge of protein-protein interactions (PPIs) is critical for understanding virus-host relationships, limitations on the scalability of high-throughput methods have hampered their identification beyond a number of well-studied viruses. Here, we implement an 〈em〉in silico〈/em〉 computational framework (pathogen host interactome prediction using structure similarity [P-HIPSTer]) that employs structural information to predict ∼282,000 pan viral-human PPIs with an experimental validation rate of ∼76%. In addition to rediscovering known biology, P-HIPSTer has yielded a series of new findings: the discovery of shared and unique machinery employed across human-infecting viruses, a likely role for ZIKV-ESR1 interactions in modulating viral replication, the identification of PPIs that discriminate between human papilloma viruses (HPVs) with high and low oncogenic potential, and a structure-enabled history of evolutionary selective pressure imposed on the human proteome. Further, P-HIPSTer enables discovery of previously unappreciated cellular circuits that act on human-infecting viruses and provides insight into experimentally intractable viruses.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0092867419308931-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 4
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    When Time Matters: An Adolescent Intervention to Prevent Adult Brain Dysfunction (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 29 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell〈/p〉 〈p〉Author(s): Sarah Canetta, Christoph Kellendonk〈/p〉 〈div〉〈p〉Can we one day prevent mental disorders? Mukherjee et al. (2019) use a genetic mouse model of schizophrenia-risk with established abnormalities in adult hippocampal-prefrontal circuit function and cognitive behaviors to identify circuit-specific treatments during adolescence that prevent the onset of the adult deficits.〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 5
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    A Cold-Sensing Receptor Encoded by a Glutamate Receptor Gene (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 29 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell〈/p〉 〈p〉Author(s): Jianke Gong, Jinzhi Liu, Elizabeth A. Ronan, Feiteng He, Wei Cai, Mahar Fatima, Wenyuan Zhang, Hankyu Lee, Zhaoyu Li, Gun-Ho Kim, Kevin P. Pipe, Bo Duan, Jianfeng Liu, X.Z. Shawn Xu〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉In search of the molecular identities of cold-sensing receptors, we carried out an unbiased genetic screen for cold-sensing mutants in 〈em〉C. elegans〈/em〉 and isolated a mutant allele of 〈em〉glr-3〈/em〉 gene that encodes a kainate-type glutamate receptor. While glutamate receptors are best known to transmit chemical synaptic signals in the CNS, we show that GLR-3 senses cold in the peripheral sensory neuron ASER to trigger cold-avoidance behavior. GLR-3 transmits cold signals via G protein signaling independently of its glutamate-gated channel function, suggesting GLR-3 as a metabotropic cold receptor. The vertebrate GLR-3 homolog GluK2 from zebrafish, mouse, and human can all function as a cold receptor in heterologous systems. Mouse DRG sensory neurons express GluK2, and GluK2 knockdown in these neurons suppresses their sensitivity to cold but not cool temperatures. Our study identifies an evolutionarily conserved cold receptor, revealing that a central chemical receptor unexpectedly functions as a thermal receptor in the periphery.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0092867419308335-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 6
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    Molecular Strategies of Meiotic Cheating by Selfish Centromeres (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 22 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell, Volume 178, Issue 5〈/p〉 〈p〉Author(s): Takashi Akera, Emily Trimm, Michael A. Lampson〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Asymmetric division in female meiosis creates selective pressure favoring selfish centromeres that bias their transmission to the egg. This centromere drive can explain the paradoxical rapid evolution of both centromere DNA and centromere-binding proteins despite conserved centromere function. Here, we define a molecular pathway linking expanded centromeres to histone phosphorylation and recruitment of microtubule destabilizing factors, leading to detachment of selfish centromeres from spindle microtubules that would direct them to the polar body. Exploiting centromere divergence between species, we show that selfish centromeres in two hybrid mouse models use the same molecular pathway but modulate it differently to enrich destabilizing factors. Our results indicate that increasing microtubule destabilizing activity is a general strategy for drive in both models, but centromeres have evolved distinct mechanisms to increase that activity. Furthermore, we show that drive depends on slowing meiotic progression, suggesting that selfish centromeres can be suppressed by regulating meiotic timing.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0092867419307408-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 7
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    Tumor Microbiome Diversity and Composition Influence Pancreatic Cancer Outcomes (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 8 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell, Volume 178, Issue 4〈/p〉 〈p〉Author(s): Erick Riquelme, Yu Zhang, Liangliang Zhang, Maria Montiel, Michelle Zoltan, Wenli Dong, Pompeyo Quesada, Ismet Sahin, Vidhi Chandra, Anthony San Lucas, Paul Scheet, Hanwen Xu, Samir M. Hanash, Lei Feng, Jared K. Burks, Kim-Anh Do, Christine B. Peterson, Deborah Nejman, Ching-Wei D. Tzeng, Michael P. Kim〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Most patients diagnosed with resected pancreatic adenocarcinoma (PDAC) survive less than 5 years, but a minor subset survives longer. Here, we dissect the role of the tumor microbiota and the immune system in influencing long-term survival. Using 16S rRNA gene sequencing, we analyzed the tumor microbiome composition in PDAC patients with short-term survival (STS) and long-term survival (LTS). We found higher alpha-diversity in the tumor microbiome of LTS patients and identified an intra-tumoral microbiome signature (〈em〉Pseudoxanthomonas〈/em〉-〈em〉Streptomyces〈/em〉-〈em〉Saccharopolyspora〈/em〉-〈em〉Bacillus clausii〈/em〉) highly predictive of long-term survivorship in both discovery and validation cohorts. Through human-into-mice fecal microbiota transplantation (FMT) experiments from STS, LTS, or control donors, we were able to differentially modulate the tumor microbiome and affect tumor growth as well as tumor immune infiltration. Our study demonstrates that PDAC microbiome composition, which cross-talks to the gut microbiome, influences the host immune response and natural history of the disease.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0092867419307731-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 8
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    A Light Touch on Sociability (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 8 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell, Volume 178, Issue 4〈/p〉 〈p〉Author(s): Nuria Domínguez-Iturza, Claudia Bagni〈/p〉 〈div〉〈p〉Autism spectrum disorder (ASD) is prevalent, complex, and heterogeneous, and currently there is no cure. Identifying shared mechanisms across the ASD spectrum is of utmost importance for therapeutic intervention. Orefice et al. show that tackling the GABA〈sub〉A〈/sub〉 receptor pathway in the peripheral somatosensory system in various ASD mouse models rescues core ASD-like phenotypes.〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 9
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    Large-Scale Analyses of Human Microbiomes Reveal Thousands of Small, Novel Genes (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 22 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell, Volume 178, Issue 5〈/p〉 〈p〉Author(s): Hila Sberro, Brayon J. Fremin, Soumaya Zlitni, Fredrik Edfors, Nicholas Greenfield, Michael P. Snyder, Georgios A. Pavlopoulos, Nikos C. Kyrpides, Ami S. Bhatt〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Small proteins are traditionally overlooked due to computational and experimental difficulties in detecting them. To systematically identify small proteins, we carried out a comparative genomics study on 1,773 human-associated metagenomes from four different body sites. We describe 〉4,000 conserved protein families, the majority of which are novel; ∼30% of these protein families are predicted to be secreted or transmembrane. Over 90% of the small protein families have no known domain and almost half are not represented in reference genomes. We identify putative housekeeping, mammalian-specific, defense-related, and protein families that are likely to be horizontally transferred. We provide evidence of transcription and translation for a subset of these families. Our study suggests that small proteins are highly abundant and those of the human microbiome, in particular, may perform diverse functions that have not been previously reported.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0092867419307810-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0092-8674
    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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  • 10
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    Align to Define: Ecologically Meaningful Populations from Genomes (2019)
    Elsevier
    In: Cell
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 8 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell, Volume 178, Issue 4〈/p〉 〈p〉Author(s): Sergey Stolyar, Christopher J. Marx〈/p〉 〈div〉〈p〉Microbes in the same community but with distinct niches can have unique long stretches of perfect sequence identity due to recent genetic exchange. Arevalo et al. (2019) use this as a starting point for defining ecologically-relevant populations within a community and to identify the genes that appear to be driving divergence between populations.〈/p〉〈/div〉
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    Electronic ISSN: 1097-4172
    Topics: Biology , Medicine
    Published by Elsevier on behalf of Cell Press.
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