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

Sent on Thursday, 2010 Sep 30
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 Sep 11;376(9744):928. How many lives does an ulcerative colitis patient have? Baumgart DC. Department of Medicine, Division of Gastroenterology and Hepatology, Charité Medical Center-Virchow Hospital, Medical School of the Humboldt-University of Berlin, Germany. daniel.baumgart@charite.de
	PMID: 20833304 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2010 Aug 28;376(9742):739-41. Epub 2010 Jul 3. The rise and fall of the antimalarial Lapdap: a lesson in pharmacogenetics. Luzzatto L. Istituto Toscano Tumori, Florence, Italy. lucio.luzzatto@ittumori.it
	PMID: 20599264 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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Sent on Saturday, 2010 Sep 25
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 Sep 2;467(7311):52-8. Integrating common and rare genetic variation in diverse human populations. International HapMap 3 Consortium, Altshuler DM, Gibbs RA, Peltonen L, Altshuler DM, Gibbs RA, Peltonen L, Dermitzakis E, Schaffner SF, Yu F, Peltonen L, Dermitzakis E, Bonnen PE, Altshuler DM, Gibbs RA, de Bakker PI, Deloukas P, Gabriel SB, Gwilliam R, Hunt S, Inouye M, Jia X, Palotie A, Parkin M, Whittaker P, Yu F, Chang K, Hawes A, Lewis LR, Ren Y, Wheeler D, Gibbs RA, Muzny DM, Barnes C, Darvishi K, Hurles M, Korn JM, Kristiansson K, Lee C, McCarrol SA, Nemesh J, Dermitzakis E, Keinan A, Montgomery SB, Pollack S, Price AL, Soranzo N, Bonnen PE, Gibbs RA, Gonzaga-Jauregui C, Keinan A, Price AL, Yu F, Anttila V, Brodeur W, Daly MJ, Leslie S, McVean G, Moutsianas L, Nguyen H, Schaffner SF, Zhang Q, Ghori MJ, McGinnis R, McLaren W, Pollack S, Price AL, Schaffner SF, Takeuchi F, Grossman SR, Shlyakhter I, Hostetter EB, Sabeti PC, Adebamowo CA, Foster MW, Gordon DR, Licinio J, Manca MC, Marshall PA, Matsuda I, Ngare D, Wang VO, Reddy D, Rotimi CN, Royal CD, Sharp RR, Zeng C, Brooks LD, McEwen JE. Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02138, USA. altshuler@molbio.mgh.harvard.edu Abstract Despite great progress in identifying genetic variants that influence human disease, most inherited risk remains unexplained. A more complete understanding requires genome-wide studies that fully examine less common alleles in populations with a wide range of ancestry. To inform the design and interpretation of such studies, we genotyped 1.6 million common single nucleotide polymorphisms (SNPs) in 1,184 reference individuals from 11 global populations, and sequenced ten 100-kilobase regions in 692 of these individuals. This integrated data set of common and rare alleles, called 'HapMap 3', includes both SNPs and copy number polymorphisms (CNPs). We characterized population-specific differences among low-frequency variants, measured the improvement in imputation accuracy afforded by the larger reference panel, especially in imputing SNPs with a minor allele frequency of <or=5%, and demonstrated the feasibility of imputing newly discovered CNPs and SNPs. This expanded public resource of genome variants in global populations supports deeper interrogation of genomic variation and its role in human disease, and serves as a step towards a high-resolution map of the landscape of human genetic variation.
	PMID: 20811451 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 Aug 5;466(7307):769-73. Epigenetic silencing of engineered L1 retrotransposition events in human embryonic carcinoma cells. Garcia-Perez JL, Morell M, Scheys JO, Kulpa DA, Morell S, Carter CC, Hammer GD, Collins KL, O'Shea KS, Menendez P, Moran JV. Department of Human Genetics, 1241 East Catherine Street, University of Michigan Medical School, Ann Arbor, Michigan 48109-5618, USA. josel.garcia.perez@juntadeandalucia.es Abstract Long interspersed element-1 (LINE-1 or L1) retrotransposition continues to affect human genome evolution. L1s can retrotranspose in the germline, during early development and in select somatic cells; however, the host response to L1 retrotransposition remains largely unexplored. Here we show that reporter genes introduced into the genome of various human embryonic carcinoma-derived cell lines (ECs) by L1 retrotransposition are rapidly and efficiently silenced either during or immediately after their integration. Treating ECs with histone deacetylase inhibitors rapidly reverses this silencing, and chromatin immunoprecipitation experiments revealed that reactivation of the reporter gene was correlated with changes in chromatin status at the L1 integration site. Under our assay conditions, rapid silencing was also observed when reporter genes were delivered into ECs by mouse L1s and a zebrafish LINE-2 element, but not when similar reporter genes were delivered into ECs by Moloney murine leukaemia virus or human immunodeficiency virus, suggesting that these integration events are silenced by distinct mechanisms. Finally, we demonstrate that subjecting ECs to culture conditions that promote differentiation attenuates the silencing of reporter genes delivered by L1 retrotransposition, but that differentiation, in itself, is not sufficient to reactivate previously silenced reporter genes. Thus, our data indicate that ECs differ from many differentiated cells in their ability to silence reporter genes delivered by L1 retrotransposition.
	PMID: 20686575 [PubMed - indexed for MEDLINE]
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3.	Nature. 2010 Aug 5;466(7307):720-6. The Amphimedon queenslandica genome and the evolution of animal complexity. Srivastava M, Simakov O, Chapman J, Fahey B, Gauthier ME, Mitros T, Richards GS, Conaco C, Dacre M, Hellsten U, Larroux C, Putnam NH, Stanke M, Adamska M, Darling A, Degnan SM, Oakley TH, Plachetzki DC, Zhai Y, Adamski M, Calcino A, Cummins SF, Goodstein DM, Harris C, Jackson DJ, Leys SP, Shu S, Woodcroft BJ, Vervoort M, Kosik KS, Manning G, Degnan BM, Rokhsar DS. Center for Integrative Genomics and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. mansi@wi.mit.edu Abstract Sponges are an ancient group of animals that diverged from other metazoans over 600 million years ago. Here we present the draft genome sequence of Amphimedon queenslandica, a demosponge from the Great Barrier Reef, and show that it is remarkably similar to other animal genomes in content, structure and organization. Comparative analysis enabled by the sequencing of the sponge genome reveals genomic events linked to the origin and early evolution of animals, including the appearance, expansion and diversification of pan-metazoan transcription factor, signalling pathway and structural genes. This diverse 'toolkit' of genes correlates with critical aspects of all metazoan body plans, and comprises cell cycle control and growth, development, somatic- and germ-cell specification, cell adhesion, innate immunity and allorecognition. Notably, many of the genes associated with the emergence of animals are also implicated in cancer, which arises from defects in basic processes associated with metazoan multicellularity.
	PMID: 20686567 [PubMed - indexed for MEDLINE]
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4.	Nature. 2010 Aug 5;466(7307):779-82. Epub 2010 Jul 18. Microbial metalloproteomes are largely uncharacterized. Cvetkovic A, Menon AL, Thorgersen MP, Scott JW, Poole FL 2nd, Jenney FE Jr, Lancaster WA, Praissman JL, Shanmukh S, Vaccaro BJ, Trauger SA, Kalisiak E, Apon JV, Siuzdak G, Yannone SM, Tainer JA, Adams MW. Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia 30602, USA. Abstract Metal ion cofactors afford proteins virtually unlimited catalytic potential, enable electron transfer reactions and have a great impact on protein stability. Consequently, metalloproteins have key roles in most biological processes, including respiration (iron and copper), photosynthesis (manganese) and drug metabolism (iron). Yet, predicting from genome sequence the numbers and types of metal an organism assimilates from its environment or uses in its metalloproteome is currently impossible because metal coordination sites are diverse and poorly recognized. We present here a robust, metal-based approach to determine all metals an organism assimilates and identify its metalloproteins on a genome-wide scale. This shifts the focus from classical protein-based purification to metal-based identification and purification by liquid chromatography, high-throughput tandem mass spectrometry (HT-MS/MS) and inductively coupled plasma mass spectrometry (ICP-MS) to characterize cytoplasmic metalloproteins from an exemplary microorganism (Pyrococcus furiosus). Of 343 metal peaks in chromatography fractions, 158 did not match any predicted metalloprotein. Unassigned peaks included metals known to be used (cobalt, iron, nickel, tungsten and zinc; 83 peaks) plus metals the organism was not thought to assimilate (lead, manganese, molybdenum, uranium and vanadium; 75 peaks). Purification of eight of 158 unexpected metal peaks yielded four novel nickel- and molybdenum-containing proteins, whereas four purified proteins contained sub-stoichiometric amounts of misincorporated lead and uranium. Analyses of two additional microorganisms (Escherichia coli and Sulfolobus solfataricus) revealed species-specific assimilation of yet more unexpected metals. Metalloproteomes are therefore much more extensive and diverse than previously recognized, and promise to provide key insights for cell biology, microbial growth and toxicity mechanisms.
	PMID: 20639861 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

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1.	N Engl J Med. 2010 Sep 16;363(12):1099-103. Preparing for a consumer-driven genomic age. Evans JP, Dale DC, Fomous C. Secretary's Advisory Committee on Genetics, Health, and Society, Washington, DC, USA.
	PMID: 20843241 [PubMed - indexed for MEDLINE]

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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 Jul 29;466(7306):632-6. Epub 2010 Jul 18. Cross-species genomics matches driver mutations and cell compartments to model ependymoma. Johnson RA, Wright KD, Poppleton H, Mohankumar KM, Finkelstein D, Pounds SB, Rand V, Leary SE, White E, Eden C, Hogg T, Northcott P, Mack S, Neale G, Wang YD, Coyle B, Atkinson J, DeWire M, Kranenburg TA, Gillespie Y, Allen JC, Merchant T, Boop FA, Sanford RA, Gajjar A, Ellison DW, Taylor MD, Grundy RG, Gilbertson RJ. Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA. Abstract Understanding the biology that underlies histologically similar but molecularly distinct subgroups of cancer has proven difficult because their defining genetic alterations are often numerous, and the cellular origins of most cancers remain unknown. We sought to decipher this heterogeneity by integrating matched genetic alterations and candidate cells of origin to generate accurate disease models. First, we identified subgroups of human ependymoma, a form of neural tumour that arises throughout the central nervous system (CNS). Subgroup-specific alterations included amplifications and homozygous deletions of genes not yet implicated in ependymoma. To select cellular compartments most likely to give rise to subgroups of ependymoma, we matched the transcriptomes of human tumours to those of mouse neural stem cells (NSCs), isolated from different regions of the CNS at different developmental stages, with an intact or deleted Ink4a/Arf locus (that encodes Cdkn2a and b). The transcriptome of human supratentorial ependymomas with amplified EPHB2 and deleted INK4A/ARF matched only that of embryonic cerebral Ink4a/Arf(-/-) NSCs. Notably, activation of Ephb2 signalling in these, but not other, NSCs generated the first mouse model of ependymoma, which is highly penetrant and accurately models the histology and transcriptome of one subgroup of human supratentorial tumour. Further, comparative analysis of matched mouse and human tumours revealed selective deregulation in the expression and copy number of genes that control synaptogenesis, pinpointing disruption of this pathway as a critical event in the production of this ependymoma subgroup. Our data demonstrate the power of cross-species genomics to meticulously match subgroup-specific driver mutations with cellular compartments to model and interrogate cancer subgroups. PMCID: PMC2912966 [Available on 2011/1/1]
	PMID: 20639864 [PubMed - indexed for MEDLINE]

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Sent on Tuesday, 2010 Sep 21
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.	Nat Genet. 2010 Sep;42(9):731-2. Infectious diseases not immune to genome-wide association. de Bakker PI, Telenti A. Comment on: Nat Genet. 2010 Sep;42(9):772-6. Nat Genet. 2010 Sep;42(9):739-41. Abstract Two genome-wide association studies for meningococcal disease and tuberculosis identify new loci associated with susceptibility to these infectious diseases. They highlight a role for the acquired and innate immune systems in host control of several human pathogens and demonstrate that denser genotyping platforms and population-specific reference panels are necessary for genetic studies in African populations.
	PMID: 20802473 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2010 Sep;42(9):745-50. Epub 2010 Aug 22. A large and complex structural polymorphism at 16p12.1 underlies microdeletion disease risk. Antonacci F, Kidd JM, Marques-Bonet T, Teague B, Ventura M, Girirajan S, Alkan C, Campbell CD, Vives L, Malig M, Rosenfeld JA, Ballif BC, Shaffer LG, Graves TA, Wilson RK, Schwartz DC, Eichler EE. Department of Genome Sciences, University of Washington, Seattle, Washington, USA. Abstract There is a complex relationship between the evolution of segmental duplications and rearrangements associated with human disease. We performed a detailed analysis of one region on chromosome 16p12.1 associated with neurocognitive disease and identified one of the largest structural inconsistencies in the human reference assembly. Various genomic analyses show that all examined humans are homozygously inverted relative to the reference genome for a 1.1-Mb region on 16p12.1. We determined that this assembly discrepancy stems from two common structural configurations with worldwide frequencies of 17.6% (S1) and 82.4% (S2). This polymorphism arose from the rapid integration of segmental duplications, precipitating two local inversions within the human lineage over the last 10 million years. The two human haplotypes differ by 333 kb of additional duplicated sequence present in S2 but not in S1. Notably, we show that the S2 configuration harbors directly oriented duplications, specifically predisposing this chromosome to disease-associated rearrangement. PMCID: PMC2930074 [Available on 2011/3/1]
	PMID: 20729854 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2010 Sep;42(9):768-71. Epub 2010 Aug 15. A genome-wide association study identifies four susceptibility loci for keloid in the Japanese population. Nakashima M, Chung S, Takahashi A, Kamatani N, Kawaguchi T, Tsunoda T, Hosono N, Kubo M, Nakamura Y, Zembutsu H. Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan. Abstract Keloid is a dermal fibroproliferative growth that results from dysfunction of the wound healing processes. Through a multistage genome-wide association study using 824 individuals with keloid (cases) and 3,205 unaffected controls in the Japanese population, we identified significant associations of keloid with four SNP loci in three chromosomal regions: 1q41, 3q22.3-23 and 15q21.3. The most significant association with keloid was observed at rs873549 (combined P = 5.89 x 10(-23), odds ratio (OR) = 1.77) on chromosome 1. Associations on chromosome 3 were observed at two separate linkage disequilibrium (LD) blocks: rs1511412 in the LD block including FOXL2 with P = 2.31 x 10(-13) (OR = 1.87) and rs940187 in another LD block with P = 1.80 x 10(-13) (OR = 1.98). Association of rs8032158 located in NEDD4 on chromosome 15 yielded P = 5.96 x 10(-13) (OR = 1.51). Our findings provide new insights into the pathophysiology of keloid formation.
	PMID: 20711176 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2010 Sep;42(9):739-41. Epub 2010 Aug 8. Genome-wide association analyses identifies a susceptibility locus for tuberculosis on chromosome 18q11.2. Thye T, Vannberg FO, Wong SH, Owusu-Dabo E, Osei I, Gyapong J, Sirugo G, Sisay-Joof F, Enimil A, Chinbuah MA, Floyd S, Warndorff DK, Sichali L, Malema S, Crampin AC, Ngwira B, Teo YY, Small K, Rockett K, Kwiatkowski D, Fine PE, Hill PC, Newport M, Lienhardt C, Adegbola RA, Corrah T, Ziegler A; African TB Genetics Consortium; Wellcome Trust Case Control Consortium, Morris AP, Meyer CG, Horstmann RD, Hill AV. Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany. Comment in: Nat Genet. 2010 Sep;42(9):731-2. Abstract We combined two tuberculosis genome-wide association studies from Ghana and The Gambia with subsequent replication in a combined 11,425 individuals. rs4331426, located in a gene-poor region on chromosome 18q11.2, was associated with disease (combined P = 6.8 x 10(-9), odds ratio = 1.19, 95% CI = 1.13-1.27). Our study demonstrates that genome-wide association studies can identify new susceptibility loci for infectious diseases, even in African populations, in which levels of linkage disequilibrium are particularly low.
	PMID: 20694014 [PubMed - indexed for MEDLINE]
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5.	Nat Genet. 2010 Sep;42(9):751-4. Epub 2010 Aug 1. Genome-wide association study identifies five new susceptibility loci for prostate cancer in the Japanese population. Takata R, Akamatsu S, Kubo M, Takahashi A, Hosono N, Kawaguchi T, Tsunoda T, Inazawa J, Kamatani N, Ogawa O, Fujioka T, Nakamura Y, Nakagawa H. Laboratory for Biomarker Development, Center of Genomic Medicine, RIKEN, Tokyo, Japan. Abstract Prostate cancer is one of the most common malignancies in males throughout the world, and its incidence is increasing in Asian countries. We carried out a genome-wide association study and replication study using 4,584 Japanese men with prostate cancer and 8,801 control subjects. From the thirty-one associated SNPs reported in previous genome-wide association studies in European populations, we confirmed the association of nine SNPs at P < 1.0 x 10(-7) and ten SNPs at P < 0.05 in the Japanese population. The remaining 12 SNPs showed no association (P > 0.05). In addition, we report here five new loci for prostate cancer susceptibility, at 5p15 (lambda-corrected probability P(GC) = 3.9 x 10(-18)), GPRC6A/RFX6 (P(GC) = 1.6 x 10(-12)), 13q22 (P(GC) = 2.8 x 10(-9)), C2orf43 (P(GC) = 7.5 x 10(-8)) and FOXP4 (P(GC) = 7.6 x 10(-8)). These findings advance our understanding of the genetic basis of prostate carcinogenesis and also highlight the genetic heterogeneity of prostate cancer susceptibility among different ethnic populations.
	PMID: 20676098 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2010 Aug 12;363(7):689-91. Sepsis and endothelial permeability. Lee WL, Slutsky AS. Keenan Research Center of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, and the Division of Respirology, University of Toronto.
	PMID: 20818861 [PubMed - indexed for MEDLINE]

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1.	Nature. 2010 Aug 26;466(7310):1029. Sugar synthesis speeds up. Van Noorden R.
	PMID: 20739977 [PubMed - indexed for MEDLINE]

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1.	Science. 2010 Aug 20;329(5994):949-53. Chloroplasts divide by contraction of a bundle of nanofilaments consisting of polyglucan. Yoshida Y, Kuroiwa H, Misumi O, Yoshida M, Ohnuma M, Fujiwara T, Yagisawa F, Hirooka S, Imoto Y, Matsushita K, Kawano S, Kuroiwa T. Laboratory of Cell Biology, Department of Life Science, College of Science, Research Information Center for Extremophile, Rikkyo University, Toshima, Tokyo 171-8501, Japan. Abstract In chloroplast division, the plastid-dividing (PD) ring is a main structure of the PD machinery and is a universal structure in the plant kingdom. However, the components and formation of the PD ring have been enigmatic. By proteomic analysis of PD machineries isolated from Cyanidioschyzon merolae, we identified the glycosyltransferase protein plastid-dividing ring 1 (PDR1), which constructs the PD ring and is widely conserved from red alga to land plants. Electron microscopy showed that the PDR1 protein forms a ring with carbohydrates at the chloroplast-division site. Fluorometric saccharide ingredient analysis of purified PD ring filaments showed that only glucose was included, and down-regulation of PDR1 impaired chloroplast division. Thus, the chloroplasts are divided by the PD ring, which is a bundle of PDR1-mediated polyglucan filaments.
	PMID: 20724635 [PubMed - indexed for MEDLINE]

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1.	Nat Med. 2010 Aug;16(8):863-4. A double agent in cancer: stopping macrophages wounds tumors. Qualls JE, Murray PJ. Department of Infectious Diseases & Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
	PMID: 20689551 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2010 Aug;16(8):861-2. A double agent in cancer: deciphering macrophage roles in human tumors. Ruhrberg C, De Palma M. UCL Institute of Ophthalmology, University College London, London, UK. c.ruhrberg@ucl.ac.uk
	PMID: 20689550 [PubMed - indexed for MEDLINE]
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