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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2010 Jun 29
Search (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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1.	J Leukoc Biol. 2010 Jun;87(6):1103-14. Epub 2010 Mar 3. Differential effects of selective HDAC inhibitors on macrophage inflammatory responses to the Toll-like receptor 4 agonist LPS. Halili MA, Andrews MR, Labzin LI, Schroder K, Matthias G, Cao C, Lovelace E, Reid RC, Le GT, Hume DA, Irvine KM, Matthias P, Fairlie DP, Sweet MJ. The University of Queensland, Institute for Molecular Bioscience, S. Lucia, Brisbane, Queensland, 4072, Australia. Abstract Broad-spectrum inhibitors of HDACs are therapeutic in many inflammatory disease models but exacerbated disease in a mouse model of atherosclerosis. HDAC inhibitors have anti- and proinflammatory effects on macrophages in vitro. We report here that several broad-spectrum HDAC inhibitors, including TSA and SAHA, suppressed the LPS-induced mRNA expression of the proinflammatory mediators Edn-1, Ccl-7/MCP-3, and Il-12p40 but amplified the expression of the proatherogenic factors Cox-2 and Pai-1/serpine1 in primary mouse BMM. Similar effects were also apparent in LPS-stimulated TEPM and HMDM. The pro- and anti-inflammatory effects of TSA were separable over a concentration range, implying that individual HDACs have differential effects on macrophage inflammatory responses. The HDAC1-selective inhibitor, MS-275, retained proinflammatory effects (amplification of LPS-induced expression of Cox-2 and Pai-1 in BMM) but suppressed only some inflammatory responses. In contrast, 17a (a reportedly HDAC6-selective inhibitor) retained anti-inflammatory but not proinflammatory properties. Despite this, HDAC6(-/-) macrophages showed normal LPS-induced expression of HDAC-dependent inflammatory genes, arguing that the anti-inflammatory effects of 17a are not a result of inhibition of HDAC6 alone. Thus, 17a provides a tool to identify individual HDACs with proinflammatory properties.
	PMID: 20200406 [PubMed - indexed for MEDLINE]

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2010 Jun 26
Search (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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1.	Nature. 2010 Jun 17;465(7300):879-80. Genomics: The tale of our other genome. Zhao L.
	PMID: 20559375 [PubMed - indexed for MEDLINE]

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2010 Jun 23
Search (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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1.	N Engl J Med. 2010 Jun 17;362(24):2328; author reply 2330-1. Comparison of dopamine and norepinephrine in shock. Romero CM. Comment on: N Engl J Med. 2010 Mar 4;362(9):779-89.
	PMID: 20554990 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jun 11;328(5984):1342. Human genetics. Who are the Jews? Genetic studies spark identity debate. Balter M.
	PMID: 20538924 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2010 Jun;16(6):638-9. Interleukin-33 safeguards neutrophils in sepsis. Roger T, Calandra T. Comment on: Nat Med. 2010 Jun;16(6):708-12.
	PMID: 20526314 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2010 Jun;16(6):708-12. Epub 2010 May 16. Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection. Alves-Filho JC, Sônego F, Souto FO, Freitas A, Verri WA Jr, Auxiliadora-Martins M, Basile-Filho A, McKenzie AN, Xu D, Cunha FQ, Liew FY. Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, UK. Comment in: Nat Med. 2010 Jun;16(6):638-9. Abstract Sepsis is a systemic inflammatory condition following bacterial infection with a high mortality rate and limited therapeutic options. Here we show that interleukin-33 (IL-33) reduces mortality in mice with experimental sepsis from cecal ligation and puncture (CLP). IL-33-treated mice developed increased neutrophil influx into the peritoneal cavity and more efficient bacterial clearance than untreated mice. IL-33 reduced the systemic but not the local proinflammatory response, and it did not induce a T helper type 1 (T(H)1) to T(H)2 shift. The chemokine receptor CXCR2 is crucial for recruitment of neutrophils from the circulation to the site of infection. Activation of Toll-like receptors (TLRs) in neutrophils downregulates CXCR2 expression and impairs neutrophil migration. We show here that IL-33 prevents the downregulation of CXCR2 and inhibition of chemotaxis induced by the activation of TLR4 in mouse and human neutrophils. Furthermore, we show that IL-33 reverses the TLR4-induced reduction of CXCR2 expression in neutrophils via the inhibition of expression of G protein-coupled receptor kinase-2 (GRK2), a serine-threonine protein kinase that induces internalization of chemokine receptors. Finally, we find that individuals who did not recover from sepsis had significantly more soluble ST2 (sST2, the decoy receptor of IL-33) than those who did recover. Together, our results indicate a previously undescribed mechanism of action of IL-33 and suggest a therapeutic potential of IL-33 in sepsis.
	PMID: 20473304 [PubMed - indexed for MEDLINE]
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5.	Science. 2010 Jun 11;328(5984):1401-3. Lysosomal pathology and osteopetrosis upon loss of H+-driven lysosomal Cl- accumulation. Weinert S, Jabs S, Supanchart C, Schweizer M, Gimber N, Richter M, Rademann J, Stauber T, Kornak U, Jentsch TJ. Leibniz-Institut für Molekulare Pharmakologie (FMP), 13125 Berlin, Germany. Comment in: Science. 2010 Jun 11;328(5984):1364-5. Abstract During lysosomal acidification, proton-pump currents are thought to be shunted by a chloride ion (Cl-) channel, tentatively identified as ClC-7. Surprisingly, recent data suggest that ClC-7 instead mediates Cl-/proton (H+) exchange. We generated mice carrying a point mutation converting ClC-7 into an uncoupled (unc) Cl- conductor. Despite maintaining lysosomal conductance and normal lysosomal pH, these Clcn7(unc/unc) mice showed lysosomal storage disease like mice lacking ClC-7. However, their osteopetrosis was milder, and they lacked a coat color phenotype. Thus, only some roles of ClC-7 Cl-/H+ exchange can be taken over by a Cl- conductance. This conductance was even deleterious in Clcn7(+/unc) mice. Clcn7(-/-) and Clcn7(unc/unc) mice accumulated less Cl- in lysosomes than did wild-type mice. Thus, lowered lysosomal chloride may underlie their common phenotypes.
	PMID: 20430974 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Thursday, 2010 Jun 17
Search (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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1.	Science. 2010 Jun 4;328(5983):1290-4. SphK1 regulates proinflammatory responses associated with endotoxin and polymicrobial sepsis. Puneet P, Yap CT, Wong L, Lam Y, Koh DR, Moochhala S, Pfeilschifter J, Huwiler A, Melendez AJ. Department of Physiology, National University of Singapore, 117597 Singapore. Abstract During sepsis, activation of phagocytes leads to the overproduction of proinflammatory cytokines, causing systemic inflammation. Despite substantial information regarding the underlying molecular mechanisms that lead to sepsis, several elements in the pathway remain to be elucidated. We found that the enzyme sphingosine kinase 1 (SphK1) is up-regulated in stimulated human phagocytes and in peritoneal phagocytes of patients with severe sepsis. Blockade of SphK1 inhibited phagocyte production of endotoxin-induced proinflammatory cytokines. We observed protection against sepsis in mice treated with a specific SphK1 inhibitor that was enhanced by treatment with a broad-spectrum antibiotic. These results demonstrated a critical role for SphK1 in endotoxin signaling and sepsis-induced inflammatory responses and suggest that inhibition of SphK1 is a potential therapy for septic shock.
	PMID: 20522778 [PubMed - indexed for MEDLINE]

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2010 Jun 16
Search (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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1.	Nature. 2010 May 13;465(7295):256-7. The sequencers. Chi KR.
	PMID: 20549837 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 May 13;465(7295):145. Genomics goes beyond DNA sequence. Katsnelson A.
	PMID: 20463710 [PubMed - indexed for MEDLINE]
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3.	Nature. 2010 Apr 29;464(7293):1362-6. Epub 2010 Mar 3. IL25 elicits a multipotent progenitor cell population that promotes T(H)2 cytokine responses. Saenz SA, Siracusa MC, Perrigoue JG, Spencer SP, Urban JF Jr, Tocker JE, Budelsky AL, Kleinschek MA, Kastelein RA, Kambayashi T, Bhandoola A, Artis D. Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. Comment in: Nature. 2010 Apr 29;464(7293):1285-6. Abstract CD4(+) T helper 2 (T(H)2) cells secrete interleukin (IL)4, IL5 and IL13, and are required for immunity to gastrointestinal helminth infections. However, T(H)2 cells also promote chronic inflammation associated with asthma and allergic disorders. The non-haematopoietic-cell-derived cytokines thymic stromal lymphopoietin, IL33 and IL25 (also known as IL17E) have been implicated in inducing T(H)2 cell-dependent inflammation at mucosal sites, but how these cytokines influence innate immune responses remains poorly defined. Here we show that IL25, a member of the IL17 cytokine family, promotes the accumulation of a lineage-negative (Lin(-)) multipotent progenitor (MPP) cell population in the gut-associated lymphoid tissue that promotes T(H)2 cytokine responses. The IL25-elicited cell population, termed MPP(type2) cells, was defined by the expression of Sca-1 (also known as Ly6a) and intermediate expression of c-Kit (c-Kit(int)), and exhibited multipotent capacity, giving rise to cells of monocyte/macrophage and granulocyte lineages both in vitro and in vivo. Progeny of MPP(type2) cells were competent antigen presenting cells, and adoptive transfer of MPP(type2) cells could promote T(H)2 cytokine responses and confer protective immunity to helminth infection in normally susceptible Il25(-/-) mice. The ability of IL25 to induce the emergence of an MPP(type2) cell population identifies a link between the IL17 cytokine family and extramedullary haematopoiesis, and suggests a previously unrecognized innate immune pathway that promotes T(H)2 cytokine responses at mucosal sites. PMCID: PMC2861732 [Available on 2010/10/29]
	PMID: 20200520 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2010 Jun 12
Search (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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1.	N Engl J Med. 2010 Jun 3;362(22):2135; author reply 2136. Macrophages in Hodgkin's lymphoma. Pazianas M. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20527079 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2010 Jun 3;362(22):2135-6; author reply 2136. Macrophages in Hodgkin's lymphoma. Kadin ME. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20527059 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2010 Jun 3;362(22):2135; author reply 2136. Macrophages in Hodgkin's lymphoma. Tsubokura M, Kodama Y, Kami M. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20519687 [PubMed - indexed for MEDLINE]
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4.	N Engl J Med. 2010 Jun 3;362(22):2092-101. Epub 2010 May 19. CISH and susceptibility to infectious d iseases. Khor CC, Vannberg FO, Chapman SJ, Guo H, Wong SH, Walley AJ, Vukcevic D, Rautanen A, Mills TC, Chang KC, Kam KM, Crampin AC, Ngwira B, Leung CC, Tam CM, Chan CY, Sung JJ, Yew WW, Toh KY, Tay SK, Kwiatkowski D, Lienhardt C, Hien TT, Day NP, Peshu N, Marsh K, Maitland K, Scott JA, Williams TN, Berkley JA, Floyd S, Tang NL, Fine PE, Goh DL, Hill AV. The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom. khorcc@gis.a-star.edu.sg Abstract BACKGROUND: The interleukin-2-mediated immune response is critical for host defense against infectious pathogens. Cytokine-inducible SRC homology 2 (SH2) domain protein (CISH), a suppressor of cytokine signaling, controls interleukin-2 signaling. METHODS: Using a case-control design, we tested for an association between CISH polymorphisms and susceptibility to major infectious diseases (bacteremia, tuberculosis, and severe malaria) in blood samples from 8402 persons in Gambia, Hong Kong, Kenya, Malawi, and Vietnam. We had previously tested 20 other immune-related genes in one or more of these sample collections. RESULTS: We observed associations between variant alleles of multiple CISH polymorphisms and increased susceptibility to each infectious disease in each of the study populations. When all five single-nucleotide polymorphisms (SNPs) (at positions -639, -292, -163, +1320, and +3415 [all relative to CISH]) within the CISH-associated locus were considered together in a multiple-SNP score, we found an association between CISH genetic variants and susceptibility to bacteremia, malaria, and tuberculosis (P=3.8x10(-11) for all comparisons), with -292 accounting for most of the association signal (P=4.58x10(-7)). Peripheral-blood mononuclear cells obtained from adult subjects carrying the -292 variant, as compared with wild-type cells, showed a muted response to the stimulation of interleukin-2 production--that is, 25 to 40% less CISH expression. CONCLUSIONS: Variants of CISH are associated with susceptibility to diseases caused by diverse infectious pathogens, suggesting that negative regulators of cytokine signaling have a role in immunity against various infectious diseases. The overall risk of one of these infectious diseases was increased by at least 18% among persons carrying the variant CISH alleles. 2010 Massachusetts Medical Society
	PMID: 20484391 [PubMed - indexed for MEDLINE]
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Sent on Friday, 2010 Jun 11
Search (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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1.	Lancet. 2010 May 1;375(9725):1525-35. Clinical assessment incorporating a personal genome. Ashley EA, Butte AJ, Wheeler MT, Chen R, Klein TE, Dewey FE, Dudley JT, Ormond KE, Pavlovic A, Morgan AA, Pushkarev D, Neff NF, Hudgins L, Gong L, Hodges LM, Berlin DS, Thorn CF, Sangkuhl K, Hebert JM, Woon M, Sagreiya H, Whaley R, Knowles JW, Chou MF, Thakuria JV, Rosenbaum AM, Zaranek AW, Church GM, Greely HT, Quake SR, Altman RB. Center for Inherited Cardiovascular Disease, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA. euan@stanford.edu Comment in: Lancet. 2010 May 1;375(9725):1497-8. Abstract BACKGROUND: The cost of genomic information has fallen steeply, but the clinical translation of genetic risk estimates remains unclear. We aimed to undertake an integrated analysis of a complete human genome in a clinical context. METHODS: We assessed a patient with a family history of vascular disease and early sudden death. Clinical assessment included analysis of this patient's full genome sequence, risk prediction for coronary artery disease, screening for causes of sudden cardiac death, and genetic counselling. Genetic analysis included the development of novel methods for the integration of whole genome and clinical risk. Disease and risk analysis focused on prediction of genetic risk of variants associated with mendelian disease, recognised drug responses, and pathogenicity for novel variants. We queried disease-specific mutation databases and pharmacogenomics databases to identify genes and mutations with known associations with disease and drug response. We estimated post-test probabilities of disease by applying likelihood ratios derived from integration of multiple common variants to age-appropriate and sex-appropriate pre-test probabilities. We also accounted for gene-environment interactions and conditionally dependent risks. FINDINGS: Analysis of 2.6 million single nucleotide polymorphisms and 752 copy number variations showed increased genetic risk for myocardial infarction, type 2 diabetes, and some cancers. We discovered rare variants in three genes that are clinically associated with sudden cardiac death-TMEM43, DSP, and MYBPC3. A variant in LPA was consistent with a family history of coronary artery disease. The patient had a heterozygous null mutation in CYP2C19 suggesting probable clopidogrel resistance, several variants associated with a positive response to lipid-lowering therapy, and variants in CYP4F2 and VKORC1 that suggest he might have a low initial dosing requirement for warfarin. Many variants of uncertain importance were reported. INTERPRETATION: Although challenges remain, our results suggest that whole-genome sequencing can yield useful and clinically relevant information for individual patients. FUNDING: National Institute of General Medical Sciences; National Heart, Lung And Blood Institute; National Human Genome Research Institute; Howard Hughes Medical Institute; National Library of Medicine, Lucile Packard Foundation for Children's Health; Hewlett Packard Foundation; Breetwor Family Foundation. Copyright 2010 Elsevier Ltd. All rights reserved.
	PMID: 20435227 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2010 May 1;375(9725):1497-8. The personal genome--the future of personalised medicine? Samani NJ, Tomaszewski M, Schunkert H. Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester LE3 9QP, UK. njs@le.ac.uk Comment on: Lancet. 2010 May 1;375(9725):1525-35.
	PMID: 20435212 [PubMed - indexed for MEDLINE]
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Sent on Thursday, 2010 Jun 10
Search (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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1.	Lancet. 2010 May 22;375(9728):1780; author reply 1780. Future diagnosis of sepsis. Chen J, Wang Y, Wang W. Comment on: Lancet. 2010 Jan 16;375(9710):224-30.
	PMID: 20494724 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2010 May 22;375(9728):1779-80; author reply 1780. Future diagnosis of sepsis. Peters RP, Savelkoul PH, Vandenbroucke-Grauls CM. Comment on: Lancet. 2010 Jan 16;375(9710):224-30.
	PMID: 20494722 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2010 Jun 09
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1.	Science. 2010 May 28;328(5982):1106. Immunology programs must include sepsis. Monneret G. Comment on: Science. 2010 Mar 26;327(5973):1573.
	PMID: 20508115 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 Apr 22;464(7292):1118-20. Environmental science: new life for the Dead Sea? Glausiusz J.
	PMID: 20414284 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2010 May 27;362(21):2028-9. Ten years on--the human genome and medicine. Varmus H.
	PMID: 20505183 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2010 May 27;362(21):2001-11. Genomic medicine--an updated primer. Feero WG, Guttmacher AE, Collins FS. National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. feerow@mail.nih.gov
	PMID: 20505179 [PubMed - indexed for MEDLINE]
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PubMed Results

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1.	Science. 2010 May 21;328(5981):994-9. A catalog of reference genomes from the human microbiome. Human Microbiome Jumpstart Reference Strains Consortium, Nelson KE, Weinstock GM, Highlander SK, Worley KC, Creasy HH, Wortman JR, Rusch DB, Mitreva M, Sodergren E, Chinwalla AT, Feldgarden M, Gevers D, Haas BJ, Madupu R, Ward DV, Birren BW, Gibbs RA, Methe B, Petrosino JF, Strausberg RL, Sutton GG, White OR, Wilson RK, Durkin S, Giglio MG, Gujja S, Howarth C, Kodira CD, Kyrpides N, Mehta T, Muzny DM, Pearson M, Pepin K, Pati A, Qin X, Yandava C, Zeng Q, Zhang L, Berlin AM, Chen L, Hepburn TA, Johnson J, McCorrison J, Miller J, Minx P, Nusbaum C, Russ C, Sykes SM, Tomlinson CM, Young S, Warren WC, Badger J, Crabtree J, Markowitz VM, Orvis J, Cree A, Ferriera S, Fulton LL, Fulton RS, Gillis M, Hemphill LD, Joshi V, Kovar C, Torralba M, Wetterstrand KA, Abouellleil A, Wollam AM, Buhay CJ, Ding Y, Dugan S, FitzGerald MG, Holder M, Hostetler J, Clifton SW, Allen-Vercoe E, Earl AM, Farmer CN, Liolios K, Surette MG, Xu Q, Pohl C, Wilczek-Boney K, Zhu D. Abstract The human microbiome refers to the community of microorganisms, including prokaryotes, viruses, and microbial eukaryotes, that populate the human body. The National Institutes of Health launched an initiative that focuses on describing the diversity of microbial species that are associated with health and disease. The first phase of this initiative includes the sequencing of hundreds of microbial reference genomes, coupled to metagenomic sequencing from multiple body sites. Here we present results from an initial reference genome sequencing of 178 microbial genomes. From 547,968 predicted polypeptides that correspond to the gene complement of these strains, previously unidentified ("novel") polypeptides that had both unmasked sequence length greater than 100 amino acids and no BLASTP match to any nonreference entry in the nonredundant subset were defined. This analysis resulted in a set of 30,867 polypeptides, of which 29,987 (approximately 97%) were unique. In addition, this set of microbial genomes allows for approximately 40% of random sequences from the microbiome of the gastrointestinal tract to be associated with organisms based on the match criteria used. Insights into pan-genome analysis suggest that we are still far from saturating microbial species genetic data sets. In addition, the associated metrics and standards used by our group for quality assurance are presented.
	PMID: 20489017 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Bacteria/classification Bacteria/genetics Bacterial Proteins/chemistry Bacterial Proteins/genetics Biodiversity Computational Biology Databases, Genetic Gastrointestinal Tract/microbiology Genes, Bacterial Genetic Variation Genome, Archaeal Genome, Bacterial* Humans Metagenome/genetics* Metagenomics/methods Metagenomics/standards Mouth/microbiology Peptides/chemistry Peptides/genetics Phylogeny Respiratory System/microbiology Sequence Analysis, DNA*/standards Skin/microbiology Urogenital System/microbiology Substances: Bacterial Proteins Peptides Grant Support: HHSN272200900017C/PHS HHS/United States N01 AI30071/AI/NIAID NIH HHS/United States U54-AI084844/AI/NIAID NIH HHS/United States U54-HG003079/HG/NHGRI NIH HHS/United States U54-HG003273/HG/NHGRI NIH HHS/United States U54-HG004968/HG/NHGRI NIH HHS/United States U54-HG004969/HG/NHGRI NIH HHS/United States U54-HG004973/HG/NHGRI NIH HHS/United States Canadian Institutes of Health Research/Canada

2.	Science. 2010 May 21;328(5981):958-9. Genomics. Synthetic genome brings new life to bacterium. Pennisi E.
	PMID: 20488994 [PubMed - indexed for MEDLINE]
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	Publication Types: News MeSH Terms: Bioengineering* Chromosomes, Bacterial* Genome, Bacterial* Genomics* Mycoplasma capricolum/genetics* Mycoplasma capricolum/growth & development Mycoplasma genitalium/genetics Mycoplasma mycoides/genetics* Mycoplasma mycoides/growth & development

3.	Nature. 2010 Apr 15;464(7291):999-1005. Genome remodelling in a basal-like breast cancer metastasis and xenograft. Ding L, Ellis MJ, Li S, Larson DE, Chen K, Wallis JW, Harris CC, McLellan MD, Fulton RS, Fulton LL, Abbott RM, Hoog J, Dooling DJ, Koboldt DC, Schmidt H, Kalicki J, Zhang Q, Chen L, Lin L, Wendl MC, McMichael JF, Magrini VJ, Cook L, McGrath SD, Vickery TL, Appelbaum E, Deschryver K, Davies S, Guintoli T, Lin L, Crowder R, Tao Y, Snider JE, Smith SM, Dukes AF, Sanderson GE, Pohl CS, Delehaunty KD, Fronick CC, Pape KA, Reed JS, Robinson JS, Hodges JS, Schierding W, Dees ND, Shen D, Locke DP, Wiechert ME, Eldred JM, Peck JB, Oberkfell BJ, Lolofie JT, Du F, Hawkins AE, O'Laughlin MD, Bernard KE, Cunningham M, Elliott G, Mason MD, Thompson DM Jr, Ivanovich JL, Goodfellow PJ, Perou CM, Weinstock GM, Aft R, Watson M, Ley TJ, Wilson RK, Mardis ER. The Genome Center at Washington University, St Louis, Missouri 63108, USA. Comment in: Nat Rev Cancer. 2010 Jun;10(6):384. Nature. 2010 Apr 15;464(7291):989-90. Abstract Massively parallel DNA sequencing technologies provide an unprecedented ability to screen entire genomes for genetic changes associated with tumour progression. Here we describe the genomic analyses of four DNA samples from an African-American patient with basal-like breast cancer: peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primary tumour. The metastasis contained two de novo mutations and a large deletion not present in the primary tumour, and was significantly enriched for 20 shared mutations. The xenograft retained all primary tumour mutations and displayed a mutation enrichment pattern that resembled the metastasis. Two overlapping large deletions, encompassing CTNNA1, were present in all three tumour samples. The differential mutation frequencies and structural variation patterns in metastasis and xenograft compared with the primary tumour indicate that secondary tumours may arise from a minority of cells within the primary tumour. PMCID: PMC2872544 [Available on 2010/10/15]
	PMID: 20393555 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Adult Brain Neoplasms/genetics* Brain Neoplasms/secondary* Breast Neoplasms/genetics* Breast Neoplasms/pathology DNA Copy Number Variations/genetics DNA Mutational Analysis Disease Progression Female Gene Frequency/genetics Genome, Human/genetics* Genomics Humans Mutation/genetics* Neoplasm Transplantation* Translocation, Genetic/genetics Transplantation, Heterologous alpha Catenin/genetics Substances: CTNNA1 protein, human alpha Catenin Grant Support: 1 U01 CA114722-01/CA/NCI NIH HHS/United States 3P50 CA68438/CA/NCI NIH HHS/United States U10 CA076001/CA/NCI NIH HHS/United States U54 HG003079/HG/NHGRI NIH HHS/United States UL1 RR024992/RR/NCRR NIH HHS/United States

4.	Nature. 2010 Apr 15;464(7291):993-8. International network of cancer genome projects. International Cancer Genome Consortium. Collaborators: Hudson TJ, Anderson W, Aretz A, Barker AD, Bell C, Bernabé RR, Bhan MK, Calvo F, Eerola I, Gerhard DS, Guttmacher A, Guyer M, Hemsley FM, Jennings JL, Kerr D, Klatt P, Kolar P, Kusuda J, Lane DP, Laplace F, Lu Y, Nettekoven G, Ozenberger B, Peterson J, Rao TS, Remacle J, Schafer AJ, Shibata T, Stratton MR, Vockley JG, Watanabe K, Yang H, Yuen MM, Knoppers BM, Bobrow M, Cambon-Thomsen A, Dressler LG, Dyke SO, Joly Y, Kato K, Kennedy KL, Nicolás P, Parker MJ, Rial-Sebbag E, Romeo-Casabona CM, Shaw KM, Wallace S, Wiesner GL, Zeps N, Lichter P, Biankin AV, Chabannon C, Chin L, Clément B, de Alava E, Degos F, Ferguson ML, Geary P, Hayes DN, Hudson TJ, Johns AL, Kasprzyk A, Nakagawa H, Penny R, Piris MA, Sarin R, Scarpa A, Shibata T, van de Vijver M, Futreal PA, Aburatani H, Bayés M, Bowtell DD, Campbell PJ, Estivill X, Gerhard DS, Grimmond SM, Gut I, Hirst M, López-Otín C, Majumder P, Marra M, McPherson JD, Nakagawa H, Ning Z, Puente XS, Ruan Y, Shibata T, Stratton MR, Stunnenberg HG, Swerdlow H, Velculescu VE, Wilson RK, Xue HH, Yang L, Spellman PT, Bader GD, Boutros PC, Campbell PJ, Flicek P, Getz G, Guigó R, Guo G, Haussler D, Heath S, Hubbard TJ, Jiang T, Jones SM, Li Q, López-Bigas N, Luo R, Muthuswamy L, Ouellette BF, Pearson JV, Puente XS, Quesada V, Raphael BJ, Sander C, Shibata T, Speed TP, Stein LD, Stuart JM, Teague JW, Totoki Y, Tsunoda T, Valencia A, Wheeler DA, Wu H, Zhao S, Zhou G, Stein LD, Guigó R, Hubbard TJ, Joly Y, Jones SM, Kasprzyk A, Lathrop M, López-Bigas N, Ouellette BF, Spellman PT, Teague JW, Thomas G, Valencia A, Yoshida T, Kennedy KL, Axton M, Dyke SO, Futreal PA, Gerhard DS, Gunter C, Guyer M, Hudson TJ, McPherson JD, Miller LJ, Ozenberger B, Shaw KM, Kasprzyk A, Stein LD, Zhang J, Haider SA, Wang J, Yung CK, Cross A, Liang Y, Gnaneshan S, Guberman J, Hsu J, Bobrow M, Chalmers DR, Hasel KW, Joly Y, Kaan TS, Kennedy KL, Knoppers BM, Lowrance WW, Masui T, Nicolás P, Rial-Sebbag E, Rodriguez LL, Vergely C, Yoshida T, Grimmond SM, Biankin AV, Bowtell DD, Cloonan N, deFazio A, Eshleman JR, Etemadmoghadam D, Gardiner BA, Kench JG, Scarpa A, Sutherland RL, Tempero MA, Waddell NJ, Wilson PJ, McPherson JD, Gallinger S, Tsao MS, Shaw PA, Petersen GM, Mukhopadhyay D, Chin L, DePinho RA, Thayer S, Muthuswamy L, Shazand K, Beck T, Sam M, Timms L, Ballin V, Lu Y, Ji J, Zhang X, Chen F, Hu X, Zhou G, Yang Q, Tian G, Zhang L, Xing X, Li X, Zhu Z, Yu Y, Yu J, Yang H, Lathrop M, Tost J, Brennan P, Holcatova I, Zaridze D, Brazma A, Egevad L, Prokhortchouk E, Banks RE, Uhlén M, Cambon-Thomsen A, Viksna J, Ponten F, Skryabin K, Stratton MR, Futreal PA, Birney E, Borg A, Børresen-Dale AL, Caldas C, Foekens JA, Martin S, Reis-Filho JS, Richardson AL, Sotiriou C, Stunnenberg HG, Thomas G, van de Vijver M, van't Veer L, Calvo F, Birnbaum D, Blanche H, Boucher P, Boyault S, Chabannon C, Gut I, Masson-Jacquemier JD, Lathrop M, Pauporté I, Pivot X, Vincent-Salomon A, Tabone E, Theillet C, Thomas G, Tost J, Treilleux I, Calvo F, Bioulac-Sage P, Clément B, Decaens T, Degos F, Franco D, Gut I, Gut M, Heath S, Lathrop M, Samuel D, Thomas G, Zucman-Rossi J, Lichter P, Eils R, Brors B, Korbel JO, Korshunov A, Landgraf P, Lehrach H, Pfister S, Radlwimmer B, Reifenberger G, Taylor MD, von Kalle C, Majumder PP, Sarin R, Rao TS, Bhan MK, Scarpa A, Pederzoli P, Lawlor RT, Delledonne M, Bardelli A, Biankin AV, Grimmond SM, Gress T, Klimstra D, Zamboni G, Shibata T, Nakamura Y, Nakagawa H, Kusuda J, Tsunoda T, Miyano S, Aburatani H, Kato K, Fujimoto A, Yoshida T, Campo E, López-Otín C, Estivill X, Guigó R, de Sanjosé S, Piris MA, Montserrat E, González-Díaz M, Puente XS, Jares P, Valencia A, Himmelbaue H, Quesada V, Bea S, Stratton MR, Futreal PA, Campbell PJ, Vincent-Salomon A, Richardson AL, Reis-Filho JS, van de Vijver M, Thomas G, Masson-Jacquemier JD, Aparicio S, Borg A, Børresen-Dale AL, Caldas C, Foekens JA, Stunnenberg HG, van't Veer L, Easton DF, Spellman PT, Martin S, Barker AD, Chin L, Collins FS, Compton CC, Ferguson ML, Gerhard DS, Getz G, Gunter C, Guttmacher A, Guyer M, Hayes DN, Lander ES, Ozenberger B, Penny R, Peterson J, Sander C, Shaw KM, Speed TP, Spellman PT, Vockley JG, Wheeler DA, Wilson RK, Hudson TJ, Chin L, Knoppers BM, Lander ES, Lichter P, Stein LD, Stratton MR, Anderson W, Barker AD, Bell C, Bobrow M, Burke W, Collins FS, Compton CC, DePinho RA, Easton DF, Futreal PA, Gerhard DS, Green AR, Guyer M, Hamilton SR, Hubbard TJ, Kallioniemi OP, Kennedy KL, Ley TJ, Liu ET, Lu Y, Majumder P, Marra M, Ozenberger B, Peterson J, Schafer AJ, Spellman PT, Stunnenberg HG, Wainwright BJ, Wilson RK, Yang H. Abstract The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
	PMID: 20393554 [PubMed - indexed for MEDLINE]
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	MeSH Terms: DNA Methylation DNA Mutational Analysis/trends Databases, Genetic Genes, Neoplasm/genetics Genetics, Medical/organization & administration* Genetics, Medical/trends Genome, Human/genetics* Genomics/organization & administration* Genomics/trends Humans Intellectual Property International Cooperation* Mutation Neoplasms/classification Neoplasms/genetics* Neoplasms/pathology Neoplasms/therapy

5.	Nature. 2010 Apr 15;464(7291):992. Obituary: Leena Peltonen-Palotie (1952-2010). van Ommen G.
	PMID: 20393553 [PubMed - indexed for MEDLINE]
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	Publication Types: Biography Historical Article News Portraits MeSH Terms: Finland Genetics, Medical/history* History, 20th Century History, 21st Century Humans Twin Studies as Topic/history Personal Name as Subject: Peltonen-Palotie L

6.	Nature. 2010 Apr 15;464(7291):989-90. Cancer: Genomics of metastasis. Gray J. Comment on: Nature. 2010 Apr 15;464(7291):999-1005.
	PMID: 20393550 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment News MeSH Terms: Adult Brain Neoplasms/genetics* Brain Neoplasms/secondary* Breast Neoplasms/genetics* Breast Neoplasms/pathology DNA Copy Number Variations/genetics DNA Mutational Analysis Disease Progression Female Gene Frequency/genetics Genome, Human/genetics* Genomics Humans Mutation/genetics* Neoplasm Transplantation* Translocation, Genetic/genetics Transplantation, Heterologous alpha Catenin/genetics Substances: CTNNA1 protein, human alpha Catenin

7.	Nature. 2010 Apr 15;464(7291):985-6. Genomics: Lessons in complexity from yeast. Goldstein DB, Noor MA. Comment on: Nature. 2010 Apr 15;464(7291):1039-42.
	PMID: 20393546 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment News MeSH Terms: Animals Chromosome Mapping/methods* Drug Resistance, Fungal/drug effects Drug Resistance, Fungal/genetics Genetic Variation/genetics* Genomics/methods* Humans Multifactorial Inheritance/genetics* Saccharomyces cerevisiae/cytology Saccharomyces cerevisiae/drug effects Saccharomyces cerevisiae/genetics* Sample Size

8.	Nature. 2010 Apr 15;464(7291):972-4. Big science: The cancer genome challenge. Ledford H.
	PMID: 20393534 [PubMed - indexed for MEDLINE]
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	Publication Types: News MeSH Terms: Cell Transformation, Neoplastic/genetics Computational Biology/trends DNA Copy Number Variations/genetics Databases, Genetic Genes, Neoplasm/genetics Genome, Human/genetics* Genomics/trends* Humans Isocitrate Dehydrogenase/genetics Neoplasms/genetics* Neoplasms/therapy Signal Transduction/genetics Substances: Isocitrate Dehydrogenase IDH1 protein, human

9.	Nature. 2010 Apr 15;464(7291):957. Testing time for gene patents. [No authors listed]
	PMID: 20393513 [PubMed - indexed for MEDLINE]
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	Publication Types: Editorial MeSH Terms: Genes* Genes, BRCA1 Genes, BRCA2 Genetic Testing/legislation & jurisprudence* Genetic Testing/trends Genetics, Medical/legislation & jurisprudence Genetics, Medical/trends Humans New York Patents as Topic/legislation & jurisprudence* Time Factors

10.	Nature. 2010 Apr 15;464(7291):1033-8. Epub 2010 Mar 28. Périgord black truffle genome uncovers evolutionary origins and mechanisms of symbiosis. Martin F, Kohler A, Murat C, Balestrini R, Coutinho PM, Jaillon O, Montanini B, Morin E, Noel B, Percudani R, Porcel B, Rubini A, Amicucci A, Amselem J, Anthouard V, Arcioni S, Artiguenave F, Aury JM, Ballario P, Bolchi A, Brenna A, Brun A, Buée M, Cantarel B, Chevalier G, Couloux A, Da Silva C, Denoeud F, Duplessis S, Ghignone S, Hilselberger B, Iotti M, Marçais B, Mello A, Miranda M, Pacioni G, Quesneville H, Riccioni C, Ruotolo R, Splivallo R, Stocchi V, Tisserant E, Viscomi AR, Zambonelli A, Zampieri E, Henrissat B, Lebrun MH, Paolocci F, Bonfante P, Ottonello S, Wincker P. INRA, UMR 1136, INRA-Nancy Université, Interactions Arbres/Microorganismes, 54280 Champenoux, France. fmartin@nancy.inra.fr Abstract The Périgord black truffle (Tuber melanosporum Vittad.) and the Piedmont white truffle dominate today's truffle market. The hypogeous fruiting body of T. melanosporum is a gastronomic delicacy produced by an ectomycorrhizal symbiont endemic to calcareous soils in southern Europe. The worldwide demand for this truffle has fuelled intense efforts at cultivation. Identification of processes that condition and trigger fruit body and symbiosis formation, ultimately leading to efficient crop production, will be facilitated by a thorough analysis of truffle genomic traits. In the ectomycorrhizal Laccaria bicolor, the expansion of gene families may have acted as a 'symbiosis toolbox'. This feature may however reflect evolution of this particular taxon and not a general trait shared by all ectomycorrhizal species. To get a better understanding of the biology and evolution of the ectomycorrhizal symbiosis, we report here the sequence of the haploid genome of T. melanosporum, which at approximately 125 megabases is the largest and most complex fungal genome sequenced so far. This expansion results from a proliferation of transposable elements accounting for approximately 58% of the genome. In contrast, this genome only contains approximately 7,500 protein-coding genes with very rare multigene families. It lacks large sets of carbohydrate cleaving enzymes, but a few of them involved in degradation of plant cell walls are induced in symbiotic tissues. The latter feature and the upregulation of genes encoding for lipases and multicopper oxidases suggest that T. melanosporum degrades its host cell walls during colonization. Symbiosis induces an increased expression of carbohydrate and amino acid transporters in both L. bicolor and T. melanosporum, but the comparison of genomic traits in the two ectomycorrhizal fungi showed that genetic predispositions for symbiosis-'the symbiosis toolbox'-evolved along different ways in ascomycetes and basidiomycetes.
	PMID: 20348908 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Ascomycota/genetics* Carbohydrates DNA Transposable Elements/genetics Evolution, Molecular* Fruiting Bodies, Fungal/metabolism Genes, Fungal/genetics Genome, Fungal/genetics* Genomics Haploidy Molecular Sequence Data Sequence Analysis, DNA Sulfur/metabolism Symbiosis/genetics* Substances: Carbohydrates DNA Transposable Elements Sulfur Secondary Source ID: GENBANK/FN429986 GENBANK/FN429987 GENBANK/FN429988 GENBANK/FN429989 GENBANK/FN429990 GENBANK/FN429991 GENBANK/FN429992 GENBANK/FN429993 GENBANK/FN429994 GENBANK/FN429995 GENBANK/FN429996 GENBANK/FN429997 GENBANK/FN429998 GENBANK/FN429999 GENBANK/FN430000 GENBANK/FN430001 GENBANK/FN430002 GENBANK/FN430003 GENBANK/FN430004 GENBANK/FN430005 GENBANK/FN430006 GENBANK/FN430007 GENBANK/FN430008 GENBANK/FN430009 GENBANK/FN430010 GENBANK/FN430011 GENBANK/FN430012 GENBANK/FN430013 GENBANK/FN430014 GENBANK/FN430015 GENBANK/FN430016 GENBANK/FN4 30017 GENBANK/FN430018 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GENBANK/FN430309 GENBANK/FN430310 GENBANK/FN430311 GENBANK/FN430312 GENBANK/FN430313 GENBANK/FN430314 GENBANK/FN430315 GENBANK/FN430316 GENBANK/FN430317 GENBANK/FN430318 GENBANK/FN430319 GENBANK/FN430320 GENBANK/FN430321 GENBANK/FN430322 GENBANK/FN430323 GENBANK/FN430324 GENBANK/FN430325 GENBANK/FN430326 GENBANK/FN430327 GENBANK/FN430328 GENBANK/FN430329 GENBANK/FN430330 GENBANK/FN430331 GENBANK/FN430332 GENBANK/FN430333 GENBANK/FN430334 GENBANK/FN430335 GENBANK/FN430336 GENBANK/FN430337 GENBANK/FN430338 GENBANK/FN430339 GENBANK/FN430340 GENBANK/FN430341 GENBANK/FN430342 GENBANK/FN430343 GENBANK/FN430344 GENBANK/FN430345 GENBANK/FN430346 GENBANK/FN430347 GENBANK/FN430348 GENBANK/FN430349 GENBANK/FN430350 GENBANK/FN430351 GENBANK/FN430352 GENBANK/FN430353 GENBANK/FN430354 GENBANK/FN430355 GENBANK/FN430356 GENBANK/FN430357 GENBANK/FN430358 GENBANK/FN430359 GENBANK/FN430360 GENBANK/FN430361 GENBANK/FN430362 GENBANK/FN430363 GENBANK/FN430364 GENBANK/FN430365 GENBANK/FN430366 GENBANK/FN430367 GENBANK/FN430368 GENBANK/FN430369 GENBANK/FN430370 GENBANK/FN430371 GENBANK/FN430372 GENBANK/FN43 0373 GENBANK/FN430374 GENBANK/FN430375 GENBANK/FN430376 GENBANK/FN430377 GENBANK/FN430378 GENBANK/FN430379 GENBANK/FN430380 GENBANK/FN430381 GENBANK/FN430382 GENBANK/FN430383 GEO/GSE17529