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

Sent on Friday, 2011 Jun 24
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. 2011 Apr 21;472(7343):303-4. Cancer: Macrophages limit chemotherapy. De Palma M, Lewis CE.
	PMID: 21512566 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Apr 21;472(7343):375-8. Epub 2011 Apr 3. Genome-wide analysis reveals novel molecular features of mouse recombination hotspots. Smagulova F, Gregoretti IV, Brick K, Khil P, Camerini-Otero RD, Petukhova GV. Source Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA. Abstract Meiotic recombination predominantly occurs at discrete genomic loci called recombination hotspots, but the features defining these areas are still largely unknown (reviewed in refs 1-5). To allow a comprehensive analysis of hotspot-associated DNA and chromatin characteristics, we developed a direct molecular approach for mapping meiotic DNA double-strand breaks that initiate recombination. Here we present the genome-wide distribution of recombination initiation sites in the mouse genome. Hotspot centres are mapped with approximately 200-nucleotide precision, which allows analysis of the fine structural details of the preferred recombination sites. We determine that hotspots share a centrally distributed consensus motif, possess a nucleotide skew that changes polarity at the centres of hotspots and have an intrinsic preference to be occupied by a nucleosome. Furthermore, we find that the vast majority of recombination initiation sites in mouse males are associated with testis-specific trimethylation of lysine 4 on histone H3 that is distinct from histone H3 lysine 4 trimethylation marks associated with transcription. The recombination map presented here has been derived from a homogeneous mouse population with a defined genetic background and therefore lends itself to extensive future experimental exploration. We note that the mapping technique developed here does not depend on the availability of genetic markers and hence can be easily adapted to other species with complex genomes. Our findings uncover several fundamental features of mammalian recombination hotspots and underline the power of the new recombination map for future studies of genetic recombination, genome stability and evolution. PMCID: PMC3117304 Free PMC Article
	PMID: 21460839 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2011 Jun 22
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. 2011 Jun 10;332(6035):1268-9. Immunology. No need to coax monocytes. Randolph GJ. Source Institute of Immunology, Mount Sinai School of Medicine, New York, NY 10029, USA. gwendalyn.randolph@mssm.edu Comment on Science. 2011 Jun 10;332(6035):1284-8.
	PMID: 21659591 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2011 Jun 11;377(9782):1982-4. Epub 2011 Jun 1. Glucocorticoid treatment in community-acquired pneumonia. Confalonieri M, Meduri GU. Source Pneumology Department, University Hospital of Trieste, Italy. marco.confalonieri@aots.sanita.fvg.it Comment on Lancet. 2011 Jun 11;377(9782):2023-30.
	PMID: 21636121 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Jun 10;332(6035):1284-8. Epub 2011 May 12. Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation. Jenkins SJ, Ruckerl D, Cook PC, Jones LH, Finkelman FD, van Rooijen N, MacDonald AS, Allen JE. Source Centre for Immunity, Infection and Evolution, and the Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. Comment in Science. 2011 Jun 10;332(6035):1268-9. Abstract A defining feature of inflammation is the accumulation of innate immune cells in the tissue that are thought to be recruited from the blood. We reveal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density. This inflammatory mechanism occurred during T helper 2 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 inflammation because exogenous IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal. Thus, expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.
	PMID: 21566158 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Apr 28;472(7344):476-80. TLR signalling augments macrophage bactericidal activity through mitochondr ial ROS. West AP, Brodsky IE, Rahner C, Woo DK, Erdjument-Bromage H, Tempst P, Walsh MC, Choi Y, Shadel GS, Ghosh S. Source Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. Abstract Reactive oxygen species (ROS) are essential components of the innate immune response against intracellular bacteria and it is thought that professional phagocytes generate ROS primarily via the phagosomal NADPH oxidase machinery. However, recent studies have suggested that mitochondrial ROS (mROS) also contribute to mouse macrophage bactericidal activity, although the mechanisms linking innate immune signalling to mitochondria for mROS generation remain unclear. Here we demonstrate that engagement of a subset of Toll-like receptors (TLR1, TLR2 and TLR4) results in the recruitment of mitochondria to macrophage phagosomes and augments mROS production. This response involves translocation of a TLR signalling adaptor, tumour necrosis factor receptor-associated factor 6 (TRAF6), to mitochondria, where it engages the protein ECSIT (evolutionarily conserved signalling intermediate in Toll pathways), which is implicated in mitochondrial respiratory chain assembly. Interaction with TRAF6 leads to ECSIT ubiquitination and enrichment at the mitochondrial periphery, resulting in increased mitochondrial and cellular ROS generation. ECSIT- and TRAF6-depleted macrophages have decreased levels of TLR-induced ROS and are significantly impaired in their ability to kill intracellular bacteria. Additionally, reducing macrophage mROS levels by expressing catalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bactericidal activity. These results reveal a novel pathway linking innate immune signalling to mitochondria, implicate mROS as an important component of antibacterial responses and further establish mitochondria as hubs for innate immune signalling.
	PMID: 21525932 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Apr 28;472(7344):471-5. Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. Goodridge HS, Reyes CN, Becker CA, Katsumoto TR, Ma J, Wolf AJ, Bose N, Chan AS, Magee AS, Danielson ME, Weiss A, Vasilakos JP, Underhill DM. Source IBD and Immunobiology Research Institute, 8700 Beverly Boulevard, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA. Abstract Innate immune cells must be able to distinguish between direct binding to microbes and detection of components shed from the surface of microbes located at a distance. Dectin-1 (also known as CLEC7A) is a pattern-recognition receptor expressed by myeloid phagocytes (macrophages, dendritic cells and neutrophils) that detects β-glucans in fungal cell walls and triggers direct cellular antimicrobial activity, including phagocytosis and production of reactive oxygen species (ROS). In contrast to inflammatory responses stimulated upon detection of soluble ligands by other pattern-recognition receptors, such as Toll-like receptors (TLRs), these responses are only useful when a cell comes into direct contact with a microbe and must not be spuriously activated by soluble stimuli. In this study we show that, despite its ability to bind both soluble and particulate β-glucan polymers, Dectin-1 signalling is only activated by particulate β-glucans, which cluster the receptor in synapse-like structures from which regulatory tyrosine phosphatases CD45 and CD148 (also known as PTPRC and PTPRJ, respectively) are excluded (Supplementary Fig. 1). The 'phagocytic synapse' now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular antimicrobial responses only when they are required. PMCID: PMC3084546 [Available on 2011/10/28]
	PMID: 21525931 [PubMed - indexed for MEDLINE]
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Sent on Friday, 2011 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.	Lancet. 2011 May 28;377(9780):1890. PAS-positive macrophages--not always infection. Meersseman W, Verschueren P, Tousseyn T, De Vos R, Cassiman D. Source Department of General Internal Medicine, University Hospital Gasthuisberg, Leuven, Belgium. wouter.meersseman@uzleuven.be
	PMID: 21621718 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2011 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.	Mol Immunol. 2011 Apr;48(8):1027-34. Epub 2011 Feb 16. The immunostimulatory activity of phosphorothioate CpG oligonucleotides is affected by distal sequence changes. Roberts TL, Dunn JA, Sweet MJ, Hume DA, Stacey KJ. Source The University of Queensland, Institute for Molecular Bioscience, Qld 4072, Australia. Tara.Roberts@qimr.edu.au Abstract CpG motifs in bacterial DNA activate innate immune cells via toll like receptor 9 (TLR9). Short synthetic oligodeoxynucleotides (ODN) containing a six base CpG motif can mimic the immunostimulatory activity of bacterial DNA. Phosphorothioate (PS) modification of the backbone of ODN makes them more resistant to nuclease degradation and consequently preferable for therapeutic use. Previous studies have shown that the sequence requirements for PS-ODN to have maximal stimulatory activity are more stringent than for normal phosphodiester (PO) ODN. Here we show small sequence changes distal to the CpG motif can affect the activity of PS-ODN whilst having no effect on the activity of PO-ODN. The addition of terminal dG residues and other minor changes to the potently immunostimulatory PS-ODN 1668S caused delayed signalling. The reduction in immunostimulatory activity of PS-ODN was associated with a delay in the activation of MAP kinases. Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.
	PMID: 21324527 [PubMed - indexed for MEDLINE]

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Sent on Friday, 2011 Jun 10
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1.	Nature. 2011 Apr 14;472(7342):179-80. Host-microbe interaction: Innate immunity cues virulence. Buckner MM, Finlay BB.
	PMID: 21490667 [PubMed - indexed for MEDLINE]

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1.	Science. 2011 May 20;332(6032):930-6. Epub 2011 Apr 21. Comparative functional genomics of the fission yeasts. Rhind N, Chen Z, Yassour M, Thompson DA, Haas BJ, Habib N, Wapinski I, Roy S, Lin MF, Heiman DI, Young SK, Furuya K, Guo Y, Pidoux A, Chen HM, Robbertse B, Goldberg JM, Aoki K, Bayne EH, Berlin AM, Desjardins CA, Dobbs E, Dukaj L, Fan L, FitzGerald MG, French C, Gujja S, Hansen K, Keifenheim D, Levin JZ, Mosher RA, Müller CA, Pfiffner J, Priest M, Russ C, Smialowska A, Swoboda P, Sykes SM, Vaughn M, Vengrova S, Yoder R, Zeng Q, Allshire R, Baulcombe D, Birren BW, Brown W, Ekwall K, Kellis M, Leatherwood J, Levin H, Margalit H, Martienssen R, Nieduszynski CA, Spatafora JW, Friedman N, Dalgaard JZ, Baumann P, Niki H, Regev A, Nusbaum C. Source Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA. nick.rhind@umassmed.edu Abstract The fission yeast clade--comprising Schizosaccharomyces pombe, S. octosporus, S. cryophilus, and S. japonicus--occupies the basal branch of Ascomycete fungi and is an important model of eukaryote biology. A comparative annotation of these genomes identified a near extinction of transposons and the associated innovation of transposon-free centromeres. Expression analysis established that meiotic genes are subject to antisense transcription during vegetative growth, which suggests a mechanism for their tight regulation. In addition, trans-acting regulators control new genes within the context of expanded functional modules for meiosis and stress response. Differences in gene content and regulation also explain why, unlike the budding yeast of Saccharomycotina, fission yeasts cannot use ethanol as a primary carbon source. These analyses elucidate the genome structure and gene regulation of fission yeast and provide tools for investigation across the Schizosaccharomyces clade.
	PMID: 21511999 [PubMed - indexed for MEDLINE]

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1.	Nat Med. 2011 Apr;17(4):401. African genomics project takes shape at Cape Town meeting. Nordling L.
	PMID: 21475220 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2011 Apr;17(4):500-3. Epub 2011 Apr 3. Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy. Collisson EA, Sadanandam A, Olson P, Gibb WJ, Truitt M, Gu S, Cooc J, Weinkle J, Kim GE, Jakkula L, Feiler HS, Ko AH, Olshen AB, Danenberg KL, Tempero MA, Spellman PT, Hanahan D, Gray JW. Source Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA. Abstract Pancreatic ductal adenocarcinoma (PDA) is a lethal disease. Overall survival is typically 6 months from diagnosis. Numerous phase 3 trials of agents effective in other malignancies have failed to benefit unselected PDA populations, although patients do occasionally respond. Studies in other solid tumors have shown that heterogeneity in response is determined, in part, by molecular differences between tumors. Furthermore, treatment outcomes are improved by targeting drugs to tumor subtypes in which they are selectively effective, with breast and lung cancers providing recent examples. Identification of PDA molecular subtypes has been frustrated by a paucity of tumor specimens available for study. We have overcome this problem by combined analysis of transcriptional profiles of primary PDA samples from several studies, along with human and mouse PDA cell lines. We define three PDA subtypes: classical, quasimesenchymal and exocrine-like, and we present evidence for clinical outcome and therapeutic response differences between them. We further define gene signatures for these subtypes that may have utility in stratifying patients for treatment and present preclinical model systems that may be used to identify new subtype specific therapies.
	PMID: 21460848 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2011 Apr;17(4):488-94. Epub 2011 Mar 20. RGMa modulates T cell responses and is involved in autoimmune encephalomyelitis. Muramatsu R, Kubo T, Mori M, Nakamura Y, Fujita Y, Akutsu T, Okuno T, Taniguchi J, Kumanogoh A, Yoshida M, Mochizuki H, Kuwabara S, Yamashita T. Source Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan. Abstract In multiple sclerosis, activated CD4(+) T cells initiate an immune response in the brain and spinal cord, resulting in demyelination, degeneration and progressive paralysis. Repulsive guidance molecule-a (RGMa) is an axon guidance molecule that has a role in the visual system and in neural tube closure. Our study shows that RGMa is expressed in bone marrow-derived dendritic cells (BMDCs) and that CD4(+) T cells express neogenin, a receptor for RGMa. Binding of RGMa to CD4(+) T cells led to activation of the small GTPase Rap1 and increased adhesion of T cells to intracellular adhesion molecule-1 (ICAM-1). Neutralizing antibodies to RGMa attenuated clinical symptoms of mouse myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) and reduced invasion of inflammatory cells into the CNS. Silencing of RGMa in MOG-pulsed BMDCs reduced their capacity to induce EAE following adoptive transfer to naive C57BL/6 mice. CD4(+) T cells isolated from mice treated with an RGMa-specific antibody showed diminished proliferative responses and reduced interferon-γ (IFN-γ), interleukin-2 (IL-2), IL-4 and IL-17 secretion. Incubation of PBMCs from patients with multiple sclerosis with an RGMa-specific antibody reduced proliferative responses and pro-inflammatory cytokine expression. These results demonstrate that an RGMa-specific antibody suppresses T cell responses, and suggest that RGMa could be a promising molecular target for the treatment of multiple sclerosis.
	PMID: 21423182 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2011 May 12;364(19):1878-9; author reply 1879. Necrotizing enterocolitis. Lin HC, Wu SF, Underwood M. Comment on N Engl J Med. 2011 Jan 20;364(3):255-64.
	PMID: 21568003 [PubMed - indexed for MEDLINE]

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1.	Nature. 2011 Apr 7;472(7341):64-8. Streptococcal M1 protein constructs a pathological host fibrinogen network. Macheboeuf P, Buffalo C, Fu CY, Zinkernagel AS, Cole JN, Johnson JE, Nizet V, Ghosh P. Source Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California 92093, USA. Abstract M1 protein, a major virulence factor of the leading invasive strain of group A Streptococcus, is sufficient to induce toxic-shock-like vascular leakage and tissue injury. These events are triggered by the formation of a complex between M1 and fibrinogen that, unlike M1 or fibrinogen alone, leads to neutrophil activation. Here we provide a structural explanation for the pathological properties of the complex formed between streptococcal M1 and human fibrinogen. A conformationally dynamic coiled-coil dimer of M1 was found to organize four fibrinogen molecules into a specific cross-like pattern. This pattern supported the construction of a supramolecular network that was required for neutrophil activation but was distinct from a fibrin clot. Disruption of this network into other supramolecular assemblies was not tolerated. These results have bearing on the pathophysiology of streptococcal toxic shock. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21475196 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Apr 7;472(7341):57-63. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, Dugar B, Feldstein AE, Britt EB, Fu X, Chung YM, Wu Y, Schauer P, Smith JD, Allayee H, Tang WH, DiDonato JA, Lusis AJ, Hazen SL. Source Department of Cell Biology, Cleveland Clinic, Cleveland, Ohio 44195, USA. Comment in Nature. 2011 Apr 7;472(7341):40-1. Abstract Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine--choline, trimethylamine N-oxide (TMAO) and betaine--were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease. ©2011 Macmillan Publishers Limited. All rights reserved PMCID: PMC3086762 [Available on 2011/10/7]
	PMID: 21475195 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Apr 7;472(7341):17. Rare-disease project has global ambitions. Abbott A.
	PMID: 21475168 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Apr 7;472(7341):90-4. Epub 2011 Mar 13. Tumour evolution inferred by single-cell sequencing. Navin N, Kendall J, Troge J, Andrews P, Rodgers L, McIndoo J, Cook K, Stepansky A, Levy D, Esposito D, Muthuswamy L, Krasnitz A, McCombie WR, Hicks J, Wigler M. Source Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. Abstract Genomic analysis provides insights into the role of copy number variation in disease, but most methods are not designed to resolve mixed populations of cells. In tumours, where genetic heterogeneity is common, very important information may be lost that would be useful for reconstructing evolutionary history. Here we show that with flow-sorted nuclei, whole genome amplification and next generation sequencing we can accurately quantify genomic copy number within an individual nucleus. We apply single-nucleus sequencing to investigate tumour population structure and evolution in two human breast cancer cases. Analysis of 100 single cells from a polygenomic tumour revealed three distinct clonal subpopulations that probably represent sequential clonal expansions. Additional analysis of 100 single cells from a monogenomic primary tumour and its liver metastasis indicated that a single clonal expansion formed the primary tumour and seeded the metastasis. In both primary tumours, we also identified an unexpectedly abundant subpopulation of genetically diverse 'pseudodiploid' cells that do not travel to the metastatic site. In contrast to gradual models of tumour progression, our data indicate that tumours grow by punctuated clonal expansions with few persistent intermediates. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21399628 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Apr 7;472(7341):115-9. Epub 2011 Mar 13. An siRNA pathway prevents transgenerational retrotransposition in plants subjected to stress. Ito H, Gaubert H, Bucher E, Mirouze M, Vaillant I, Paszkowski J. Source Department of Plant Biology, University of Geneva, Sciences III, 30 Quai Ernest-Ansermet, CH-1211 Geneva 4, Switzerland. Abstract Eukaryotic genomes consist to a significant extent of retrotransposons that are suppressed by host epigenetic mechanisms, preventing their uncontrolled propagation. However, it is not clear how this is achieved. Here we show that in Arabidopsis seedlings subjected to heat stress, a copia-type retrotransposon named ONSEN (Japanese 'hot spring') not only became transcriptionally active but also synthesized extrachromosomal DNA copies. Heat-induced ONSEN accumulation was stimulated in mutants impaired in the biogenesis of small interfering RNAs (siRNAs); however, there was no evidence of transposition occurring in vegetative tissues. After stress, both ONSEN transcripts and extrachromosomal DNA gradually decayed and were no longer detected after 20-30 days. Surprisingly, a high frequency of new ONSEN insertions was observed in the progeny of stressed plants deficient in siRNAs. Insertion patterns revealed that this transgenerational retrotransposition occurred during flower development and before gametogenesis. Therefore in plants with compromised siRNA biogenesis, memory of stress was maintained throughout development, priming ONSEN to transpose during differentiation of generative organs. Retrotransposition was not observed in the progeny of wild-type plants subjected to stress or in non-stressed mutant controls, pointing to a crucial role of the siRNA pathway in restricting retrotransposition triggered by environmental stress. Finally, we found that natural and experimentally induced variants in ONSEN insertions confer heat responsiveness to nearby genes, and therefore mobility bursts may generate novel, stress-responsive regulatory gene networks. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21399627 [PubMed - indexed for MEDLINE]
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6.	J Leukoc Biol. 2011 Apr;89(4):525-38. Epub 2010 Dec 17. Applications of myeloid-specific promoters in transgenic mice support in vivo imaging and functional genomics but do not su pport the concept of distinct macrophage and dendritic cell lineages or roles in immunity. Hume DA. Source The Roslin Institute, University of Edinburgh, Roslin, Midlothian EH25 9PS, UK. david.hume@roslin.ed.ac.uk Abstract Myeloid lineage cells contribute to innate and acquired immunity, homeostasis, wound repair, and inflammation. There is considerable interest in manipulation of their function in transgenic mice using myeloid-specific promoters. This review considers the applications and specificity of some of the most widely studied transgenes, driven by promoter elements of the lysM, csf1r, CD11c, CD68, macrophage SRA, and CD11b genes, as well as several others. Transgenes have been used in mice to generate myeloid lineage-specific cell ablation, expression of genes of interest, including fluorescent reporters, or deletion via recombination. In general, the specificity of such transgenes has been overinterpreted, and none of them provide well-documented, reliable, differential expression in any specific myeloid cell subset, macrophages, granulocytes, or myeloid DCs. Nevertheless, they have proved valuable in cell isolation, functional genomics, and live imaging of myeloid cell behavior in many different pathologies.
	PMID: 21169519 [PubMed - indexed for MEDLINE]
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