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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Tuesday, 2013 December 17Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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| PubMed Results |
| 1. | N Engl J Med. 2013 Nov 21;369(21):2063. doi: 10.1056/NEJMc1312359#SA3.Severe sepsis and septic shock.Moreira J.Comment in
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| PMID: 24256393 [PubMed - in process] | |
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| 2. | N Engl J Med. 2013 Nov 21;369(21):2062-3. doi: 10.1056/NEJMc1312359#SA2.Severe sepsis and septic shock.De Blasi RA.Comment in
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| PMID: 24256392 [PubMed - in process] | |
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| 3. | N Engl J Med. 2013 Nov 21;369(21):2062. doi: 10.1056/NEJMc1312359#SA1.Severe sepsis and septic shock.Calis J, van Woensel J, Lemson J.Comment in
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| PMID: 24256391 [PubMed - in process] | |
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| 4. | N Engl J Med. 2013 Nov 21;369(21):2063. doi: 10.1056/NEJMc1312359.Severe sepsis and septic shock.Angus DC, van der Poll T.Comment on
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| PMID: 24256390 [PubMed - in process] | |
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| 5. | Science. 2013 Nov 15;342(6160):863-6. doi: 10.1126/science.1242255.Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death.Thammavongsa V, Missiakas DM, Schneewind O.Department of Microbiology, University of Chicago, 920 East 58th Street, Chicago, IL 60637, USA. AbstractBacterial invasion of host tissues triggers polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microbes for subsequent clearance by innate defenses including macrophage phagocytosis. We report here that Staphylococcus aureus escapes these defenses by converting NETs to deoxyadenosine, which triggers the caspase-3-mediated death of immune cells. Conversion of NETs to deoxyadenosine requires two enzymes, nuclease and adenosine synthase, that are secreted by S. aureus and are necessary for the exclusion of macrophages from staphylococcal abscesses. Thus, the pathogenesis of S. aureus infections has evolved to anticipate host defenses and to repurpose them for the destruction of the immune system. |
| PMID: 24233725 [PubMed - in process] | |
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| 6. | Lancet. 2013 Oct 26;382(9902):1398. doi: 10.1016/S0140-6736(13)62204-7. Epub 2013 Oct 25.Anthony James Pawson.Watts G. |
| PMID: 24206610 [PubMed - in process] | |
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| 7. | Science. 2013 Nov 8;342(6159):699-700. doi: 10.1126/science.1244270.Cancer. Fusion for moving.Clawson GA.Gittlen Cancer Research Foundation, Department of Pathology, and Department of Biochemistry & Molecular Biology, Hershey Medical Center, Pennsylvania State University, Hershey, PA 17033, USA. |
| PMID: 24202164 [PubMed - in process] | |
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| 8. | Nature. 2013 Oct 31;502(7473):617-8.Climate change: Melting glaciers bring energy uncertainty.Laghari JR.Comment in
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| PMID: 24180016 [PubMed - in process] | |
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| 9. | Nature. 2013 Nov 14;503(7475):224-8. doi: 10.1038/nature12744. Epub 2013 Oct 30.Therapeutic efficacy of potent neutralizing HIV-1-specific monoclonal antibodies in SHIV-infected rhesus monkeys.Barouch DH, Whitney JB, Moldt B, Klein F, Oliveira TY, Liu J, Stephenson KE, Chang HW, Shekhar K, Gupta S, Nkolola JP, Seaman MS, Smith KM, Borducchi EN, Cabral C, Smith JY, Blackmore S, Sanisetty S, Perry JR, Beck M, Lewis MG, Rinaldi W, Chakraborty AK, Poignard P, Nussenzweig MC, Burton DR.1] Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts 02139, USA. Comment in
AbstractHuman immunodeficiency virus type 1 (HIV-1)-specific monoclonal antibodies with extraordinary potency and breadth have recently been described. In humanized mice, combinations of monoclonal antibodies have been shown to suppress viraemia, but the therapeutic potential of these monoclonal antibodies has not yet been evaluated in primates with an intact immune system. Here we show that administration of a cocktail of HIV-1-specific monoclonal antibodies, as well as the single glycan-dependent monoclonal antibody PGT121, resulted in a rapid and precipitous decline of plasma viraemia to undetectable levels in rhesus monkeys chronically infected with the pathogenic simian-human immunodeficiency virus SHIV-SF162P3. A single monoclonal antibody infusion afforded up to a 3.1 log decline of plasma viral RNA in 7 days and also reduced proviral DNA in peripheral blood, gastrointestinal mucosa and lymph nodes without the development of viral resistance. Moreover, after monoclonal antibody administration, host Gag-specific T-lymphocyte responses showed improved functionality. Virus rebounded in most animals after a median of 56 days when serum monoclonal antibody titres had declined to undetectable levels, although, notably, a subset of animals maintained long-term virological control in the absence of further monoclonal antibody infusions. These data demonstrate a profound therapeutic effect of potent neutralizing HIV-1-specific monoclonal antibodies in SHIV-infected rhesus monkeys as well as an impact on host immune responses. Our findings strongly encourage the investigation of monoclonal antibody therapy for HIV-1 in humans. |
| PMID: 24172905 [PubMed - in process] | |
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| 10. | Nature. 2013 Nov 14;503(7475):277-80. doi: 10.1038/nature12746. Epub 2013 Oct 30.Antibody-mediated immunotherapy of macaques chronically infected with SHIV suppresses viraemia.Shingai M, Nishimura Y, Klein F, Mouquet H, Donau OK, Plishka R, Buckler-White A, Seaman M, Piatak M Jr, Lifson JD, Dimitrov DS, Nussenzweig MC, Martin MA.1] Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. Comment in
AbstractNeutralizing antibodies can confer immunity to primate lentiviruses by blocking infection in macaque models of AIDS. However, earlier studies of anti-human immunodeficiency virus type 1 (HIV-1) neutralizing antibodies administered to infected individuals or humanized mice reported poor control of virus replication and the rapid emergence of resistant variants. A new generation of anti-HIV-1 monoclonal antibodies, possessing extraordinary potency and breadth of neutralizing activity, has recently been isolated from infected individuals. These neutralizing antibodies target different regions of the HIV-1 envelope glycoprotein including the CD4-binding site, glycans located in the V1/V2, V3 and V4 regions, and the membrane proximal external region of gp41 (refs 9-14). Here we have examined two of the new antibodies, directed to the CD4-binding site and the V3 region (3BNC117 and 10-1074, respectively), for their ability to block infection and suppress viraemia in macaques infected with the R5 tropic simian-human immunodeficiency virus (SHIV)-AD8, which emulates many of the pathogenic and immunogenic properties of HIV-1 during infections of rhesus macaques. Either antibody alone can potently block virus acquisition. When administered individually to recently infected macaques, the 10-1074 antibody caused a rapid decline in virus load to undetectable levels for 4-7 days, followed by virus rebound during which neutralization-resistant variants became detectable. When administered together, a single treatment rapidly suppressed plasma viraemia for 3-5 weeks in some long-term chronically SHIV-infected animals with low CD4(+) T-cell levels. A second cycle of anti-HIV-1 monoclonal antibody therapy, administered to two previously treated animals, successfully controlled virus rebound. These results indicate that immunotherapy or a combination of immunotherapy plus conventional antiretroviral drugs might be useful as a treatment for chronically HIV-1-infected individuals experiencing immune dysfunction. |
| PMID: 24172896 [PubMed - in process] | |
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| 11. | Nature. 2013 Nov 14;503(7475):207-8. doi: 10.1038/nature12703. Epub 2013 Oct 30.HIV: Antibodies advance the search for a cure.Picker LJ, Deeks SG.Vaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton, Oregon 97006, USA. |
| PMID: 24172894 [PubMed - in process] | |
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| 12. | Science. 2013 Oct 18;342(6156):326-31. doi: 10.1126/science.1238484.A complete skull from Dmanisi, Georgia, and the evolutionary biology of early Homo.Lordkipanidze D, Ponce de León MS, Margvelashvili A, Rak Y, Rightmire GP, Vekua A, Zollikofer CP.Georgian National Museum, 3 Purtseladze Street, 0105 Tbilisi, Georgia. Comment in
AbstractThe site of Dmanisi, Georgia, has yielded an impressive sample of hominid cranial and postcranial remains, documenting the presence of Homo outside Africa around 1.8 million years ago. Here we report on a new cranium from Dmanisi (D4500) that, together with its mandible (D2600), represents the world's first completely preserved adult hominid skull from the early Pleistocene. D4500/D2600 combines a small braincase (546 cubic centimeters) with a large prognathic face and exhibits close morphological affinities with the earliest known Homo fossils from Africa. The Dmanisi sample, which now comprises five crania, provides direct evidence for wide morphological variation within and among early Homo paleodemes. This implies the existence of a single evolving lineage of early Homo, with phylogeographic continuity across continents. |
| PMID: 24136960 [PubMed - in process] | |
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| 13. | Science. 2013 Oct 18;342(6156):321-3. doi: 10.1126/science.1244869.Paleontology. Did the Denisovans cross Wallace's Line?Cooper A, Stringer CB.Australian Centre for Ancient DNA, University of Adelaide, Adelaide 5005, South Australia. |
| PMID: 24136958 [PubMed - in process] | |
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| 14. | Nature. 2013 Oct 17;502(7471):317-20. doi: 10.1038/nature12564.Criteria for the use of omics-based predictors in clinical trials.McShane LM, Cavenagh MM, Lively TG, Eberhard DA, Bigbee WL, Williams PM, Mesirov JP, Polley MY, Kim KY, Tricoli JV, Taylor JM, Shuman DJ, Simon RM, Doroshow JH, Conley BA.Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. mcshanel@ctep.nci.nih.gov AbstractThe US National Cancer Institute (NCI), in collaboration with scientists representing multiple areas of expertise relevant to 'omics'-based test development, has developed a checklist of criteria that can be used to determine the readiness of omics-based tests for guiding patient care in clinical trials. The checklist criteria cover issues relating to specimens, assays, mathematical modelling, clinical trial design, and ethical, legal and regulatory aspects. Funding bodies and journals are encouraged to consider the checklist, which they may find useful for assessing study quality and evidence strength. The checklist will be used to evaluate proposals for NCI-sponsored clinical trials in which omics tests will be used to guide therapy. |
| PMID: 24132288 [PubMed - in process] | |
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| 15. | Nature. 2013 Oct 10;502(7470):143. doi: 10.1038/502143a.Improving genome understanding.Church G.Harvard Medical School, Boston, Massachusetts, USA. gmc@harvard.edu Erratum in
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| PMID: 24108012 [PubMed - in process] | |
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| 16. | Nature. 2013 Sep 12;501(7466):135.Sequenced from the start.[No authors listed] |
| PMID: 24032129 [PubMed - in process] | |
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| 17. | Nature. 2013 Sep 12;501(7466):263-8. doi: 10.1038/501261a.Next-generation sequencing: The genome jigsaw.Marx V. |
| PMID: 24025842 [PubMed - in process] | |
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| 18. | Nat Med. 2013 Sep;19(9):1094-5. doi: 10.1038/nm.3316.Proliferating macrophages prevail in atherosclerosis.Randolph GJ.Department of Pathology and Immunology at Washington University School of Medicine, St. Louis, Missouri, USA. Comment onAbstractMacrophages accumulate in atherosclerotic lesions during the inflammation that is part of atherosclerosis development and progression. A new study in mice indicates that the accumulation of macrophages in atherosclerotic plaques depends on local macrophage proliferation rather than the recruitment of circulating monocytes. |
| PMID: 24013746 [PubMed - in process] | |
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| 19. | Nat Med. 2013 Sep;19(9):1073. doi: 10.1038/nm.3342.Privacy and protection in the genomic era.[No authors listed] |
| PMID: 24013730 [PubMed - in process] | |
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| 20. | Nature. 2013 Sep 5;501(7465):14-5. doi: 10.1038/501014a.Floods spur mountain study.Qiu J. |
| PMID: 24005394 [PubMed - in process] | |
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| 21. | Nat Genet. 2013 Sep;45(9):963. doi: 10.1038/ng.2755.Nuclear reprogramming and the cancer genome.[No authors listed] |
| PMID: 23985680 [PubMed - in process] | |
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| 22. | Nat Med. 2013 Sep;19(9):1132-40. doi: 10.1038/nm.3265. Epub 2013 Aug 18.Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids mediates beta cell loss in type 2 diabetes.Jourdan T, Godlewski G, Cinar R, Bertola A, Szanda G, Liu J, Tam J, Han T, Mukhopadhyay B, Skarulis MC, Ju C, Aouadi M, Czech MP, Kunos G.Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, Bethesda, Maryland. AbstractType 2 diabetes mellitus (T2DM) progresses from compensated insulin resistance to beta cell failure resulting in uncompensated hyperglycemia, a process replicated in the Zucker diabetic fatty (ZDF) rat. The Nlrp3 inflammasome has been implicated in obesity-induced insulin resistance and beta cell failure. Endocannabinoids contribute to insulin resistance through activation of peripheral CB1 receptors (CB₁Rs) and also promote beta cell failure. Here we show that beta cell failure in adult ZDF rats is not associated with CB₁R signaling in beta cells, but rather in M1 macrophages infiltrating into pancreatic islets, and that this leads to activation of the Nlrp3-ASC inflammasome in the macrophages. These effects are replicated in vitro by incubating wild-type human or rodent macrophages, but not macrophages from CB₁R-deficient (Cnr1(-/-)) or Nlrp3(-/-) mice, with the endocannabinoid anandamide. Peripheral CB₁R blockade, in vivo depletion of macrophages or macrophage-specific knockdown of CB₁R reverses or prevents these changes and restores normoglycemia and glucose-induced insulin secretion. These findings implicate endocannabinoids and inflammasome activation in beta cell failure and identify macrophage-expressed CB₁R as a therapeutic target in T2DM. |
| PMID: 23955712 [PubMed - in process] | |
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| 23. | Nat Med. 2013 Sep;19(9):1166-72. doi: 10.1038/nm.3258. Epub 2013 Aug 11.Local proliferation dominates lesional macrophage accumulation in atherosclerosis.Robbins CS, Hilgendorf I, Weber GF, Theurl I, Iwamoto Y, Figueiredo JL, Gorbatov R, Sukhova GK, Gerhardt LM, Smyth D, Zavitz CC, Shikatani EA, Parsons M, van Rooijen N, Lin HY, Husain M, Libby P, Nahrendorf M, Weissleder R, Swirski FK.1] Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. [2] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [3] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. [4] Department of Immunology, University of Toronto, Toronto, Ontario, Canada. [5]. Comment in
AbstractDuring the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall. The observation that circulating monocytes give rise to lesional macrophages has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts. We therefore revisited the mechanism underlying macrophage accumulation in atherosclerosis. In murine atherosclerotic lesions, we found that macrophages turn over rapidly, after 4 weeks. Replenishment of macrophages in these experimental atheromata depends predominantly on local macrophage proliferation rather than monocyte influx. The microenvironment orchestrates macrophage proliferation through the involvement of scavenger receptor A (SR-A). Our study reveals macrophage proliferation as a key event in atherosclerosis and identifies macrophage self-renewal as a therapeutic target for cardiovascular disease. |
| PMID: 23933982 [PubMed - in process] | |
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| 24. | Nature. 2013 Sep 12;501(7466):237-41. doi: 10.1038/nature12427. Epub 2013 Jul 31.Completion of the entire hepatitis C virus life cycle in genetically humanized mice.Dorner M, Horwitz JA, Donovan BM, Labitt RN, Budell WC, Friling T, Vogt A, Catanese MT, Satoh T, Kawai T, Akira S , Law M, Rice CM, Ploss A.Center for the Study of Hepatitis C, The Rockefeller University, New York, New York 10065, USA. Comment in
AbstractMore than 130 million people worldwide chronically infected with hepatitis C virus (HCV) are at risk of developing severe liver disease. Antiviral treatments are only partially effective against HCV infection, and a vaccine is not available. Development of more efficient therapies has been hampered by the lack of a small animal model. Building on the observation that CD81 and occludin (OCLN) comprise the minimal set of human factors required to render mouse cells permissive to HCV entry, we previously showed that transient expression of these two human genes is sufficient to allow viral uptake into fully immunocompetent inbred mice. Here we demonstrate that transgenic mice stably expressing human CD81 and OCLN also support HCV entry, but innate and adaptive immune responses restrict HCV infection in vivo. Blunting antiviral immunity in genetically humanized mice infected with HCV results in measurable viraemia over several weeks. In mice lacking the essential cellular co-factor cyclophilin A (CypA), HCV RNA replication is markedly diminished, providing genetic evidence that this process is faithfully recapitulated. Using a cell-based fluorescent reporter activated by the NS3-4A protease we visualize HCV infection in single hepatocytes in vivo. Persistently infected mice produce de novo infectious particles, which can be inhibited with directly acting antiviral drug treatment, thereby providing evidence for the completion of the entire HCV life cycle in inbred mice. This genetically humanized mouse model opens new opportunities to dissect genetically HCV infection in vivo and provides an important preclinical platform for testing and prioritizing drug candidates and may also have utility for evaluating vaccine efficacy. |
| PMID: 23903655 [PubMed - in process] | |
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| 25. | Nat Genet. 2013 Sep;45(9):1083-7. doi: 10.1038/ng.2705. Epub 2013 Jul 21.Independent specialization of the human and mouse X chromosomes for the male germ line.Mueller JL, Skaletsky H, Brown LG, Zaghlul S, Rock S, Graves T, Auger K, Warren WC, Wilson RK, Page DC.Whitehead Institute, Cambridge, Massachusetts, USA. AbstractWe compared the human and mouse X chromosomes to systematically test Ohno's law, which states that the gene content of X chromosomes is conserved across placental mammals. First, we improved the accuracy of the human X-chromosome reference sequence through single-haplotype sequencing of ampliconic regions. The new sequence closed gaps in the reference sequence, corrected previously misassembled regions and identified new palindromic amplicons. Our subsequent analysis led us to conclude that the evolution of human and mouse X chromosomes was bimodal. In accord with Ohno's law, 94-95% of X-linked single-copy genes are shared by humans and mice; most are expressed in both sexes. Notably, most X-ampliconic genes are exceptions to Ohno's law: only 31% of human and 22% of mouse X-ampliconic genes had orthologs in the other species. X-ampliconic genes are expressed predominantly in testicular germ cells, and many were independently acquired since divergence from the common ancestor of humans and mice, specializing portions of their X chromosomes for sperm production. |
| PMID: 23872635 [PubMed - in process] | |
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| 26. | J Biol Chem. 2013 Aug 30;288(35):25362-74. doi: 10.1074/jbc.M113.496281. Epub 2013 Jul 12.Histone deacetylase 7 promotes Toll-like receptor 4-dependent proinflammatory gene expression in macrophages.Shakespear MR, Hohenhaus DM, Kelly GM, Kamal NA, Gupta P, Labzin LI, Schroder K, Garceau V, Barbero S, Iyer A, Hume DA, Reid RC, Irvine KM, Fairlie DP, Sweet MJ.Institute for Molecular Bioscience and Australian Infectious Diseases Research Centre, University of Queensland, Queensland 4072, Australia. AbstractBroad-spectrum inhibitors of histone deacetylases (HDACs) constrain Toll-like receptor (TLR)-inducible production of key proinflammatory mediators. Here we investigated HDAC-dependent inflammatory responses in mouse macrophages. Of the classical Hdacs, Hdac7 was expressed at elevated levels in inflammatory macrophages (thioglycollate-elicited peritoneal macrophages) as compared with bone marrow-derived macrophages and the RAW264 cell line. Overexpression of a specific, alternatively spliced isoform of Hdac7 lacking the N-terminal 22 amino acids (Hdac7-u), but not the Refseq Hdac7 (Hdac7-s), promoted LPS-inducible expression of Hdac-dependent genes (Edn1, Il-12p40, and Il-6) in RAW264 cells. A novel class IIa-selective HDAC inhibitor reduced recombinant human HDAC7 enzyme activity as well as TLR-induced production of inflammatory mediators in thioglycollate-elicited peritoneal macrophages. Both LPS and Hdac7-u up-regulated the activity of the Edn1 promoter in an HDAC-dependent fashion in RAW264 cells. A hypoxia-inducible factor (HIF) 1 binding site in this promoter was required for HDAC-dependent TLR-inducible promoter activity and for Hdac7- and HIF-1α-mediated trans-activation. Coimmunoprecipitation assays showed that both Hdac7-u and Hdac7-s interacted with HIF-1α, whereas only Hdac7-s interacted with the transcriptional repressor CtBP1. Thus, Hdac7-u positively regulates HIF-1α-dependent TLR signaling in macrophages, whereas an interaction with CtBP1 likely prevents Hdac7-s from exerting this effect. Hdac7 may represent a potential inflammatory disease target. |
| PMID: 23853092 [PubMed - in process] | |
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| 27. | Nat Genet. 2013 Sep;45(9):970-6. doi: 10.1038/ng.2702. Epub 2013 Jul 14.An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers.Roberts SA, Lawrence MS, Klimczak LJ, Grimm SA, Fargo D, Stojanov P, Kiezun A, Kryukov GV, Carter SL, Saksena G, Harris S, Shah RR, Resnick MA, Getz G, Gordenin DA.Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Durham, North Carolina, USA. Comment in
AbstractRecent studies indicate that a subclass of APOBEC cytidine deaminases, which convert cytosine to uracil during RNA editing and retrovirus or retrotransposon restriction, may induce mutation clusters in human tumors. We show here that throughout cancer genomes APOBEC-mediated mutagenesis is pervasive and correlates with APOBEC mRNA levels. Mutation clusters in whole-genome and exome data sets conformed to the stringent criteria indicative of an APOBEC mutation pattern. Applying these criteria to 954,247 mutations in 2,680 exomes from 14 cancer types, mostly from The Cancer Genome Atlas (TCGA), showed a significant presence of the APOBEC mutation pattern in bladder, cervical, breast, head and neck, and lung cancers, reaching 68% of all mutations in some samples. Within breast cancer, the HER2-enriched subtype was clearly enriched for tumors with the APOBEC mutation pattern, suggesting that this type of mutagenesis is functionally linked with cancer development. The APOBEC mutation pattern also extended to cancer-associated genes, implying that ubiquitous APOBEC-mediated mutagenesis is carcinogenic. |
| PMID: 23852170 [PubMed - in process] | |
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| 28. | Nat Genet. 2013 Sep;45(9):1029-39. doi: 10.1038/ng.2703. Epub 2013 Jul 14.Reconstructing de novo silencing of an active plant retrotransposon.Marí-Ordóñez A, Marchais A, Etcheverry M, Martin A, Colot V, Voinnet O.Swiss Federal Institute of Technology (ETH-Z), Department of Biology, Zurich, Switzerland. AbstractTransposable elements (TEs) contribute to genome size, organization and evolution. In plants, their activity is primarily controlled by transcriptional gene silencing (TGS), usually investigated at steady states, reflecting how long-established silent conditions are maintained, faithfully reiterated or temporarily modified. How active, invasive TEs are detected and silenced de novo in plants remains largely unknown. Using inbred lineages of hybrid Arabidopsis thaliana epigenomes combining wild-type and mutant chromosomes, we have deciphered the sequence of physiological and molecular events underlying the de novo invasion, proliferation and eventual demise of the single-copy endogenous retrotransposon Evadé (EVD). We show how this reconstructed TE burst causes widespread genome diversification and de novo epiallelism that could serve as sources for selectable and potentially adaptive traits. |
| PMID: 23852169 [PubMed - in process] | |
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| 29. | Nat Genet. 2013 Sep;45(9):1092-6. doi: 10.1038/ng.2704. Epub 2013 Jul 14.The wheat powdery mildew genome shows the unique evolution of an obligate biotroph.Wicker T, Oberhaensli S, Parlange F, Buchmann JP, Shatalina M, Roffler S, Ben-David R, Doležel J, Šimková H, Schulze-Lefert P, Spanu PD, Bruggmann R, Amselem J, Quesneville H, Ver Loren van Themaat E, Paape T, Shimizu KK, Keller B.Institute of Plant Biology, University of Zurich, Zurich, Switzerland. wicker@botinst.uzh.ch AbstractWheat powdery mildew, Blumeria graminis forma specialis tritici, is a devastating fungal pathogen with a poorly understood evolutionary history. Here we report the draft genome sequence of wheat powdery mildew, the resequencing of three additional isolates from different geographic regions and comparative analyses with the barley powdery mildew genome. Our comparative genomic analyses identified 602 candidate effector genes, with many showing evidence of positive selection. We characterize patterns of genetic diversity and suggest that mildew genomes are mosaics of ancient haplogroups that existed before wheat domestication. The patterns of diversity in modern isolates suggest that there was no pronounced loss of genetic diversity upon formation of the new host bread wheat 10,000 years ago. We conclude that the ready adaptation of B. graminis f.sp. tritici to the new host species was based on a diverse haplotype pool that provided great genetic potential for pathogen variation. |
| PMID: 23852167 [PubMed - in process] | |
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