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  • 1
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    Multimodal warning signals for a multiple predator world (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-09-05
    Description: Aposematism is an anti-predator defence, dependent on a predator's ability to associate unprofitable prey with a prey-borne signal. Multimodal signals should vary in efficacy according to the sensory systems of different predators; however, until now, the impact of multiple predator classes on the evolution of these signals had not been investigated. Here, using a community-level molecular phylogeny to generate phylogenetically independent contrasts, we show that warning signals of tiger moths vary according to the seasonal and daily activity patterns of birds and bats-predators with divergent sensory capacities. Many tiger moths advertise chemical defence using conspicuous colouration and/or ultrasonic clicks. During spring, when birds are active and bats less so, we found that tiger moths did not produce ultrasonic clicks. Throughout both spring and summer, tiger moths most active during the day were visually conspicuous. Those species emerging later in the season produced ultrasonic clicks; those that were most nocturnal were visually cryptic. Our results indicate that selective pressures from multiple predator classes have distinct roles in the evolution of multimodal warning displays now effective against a single predator class. We also suggest that the evolution of acoustic warning signals may lack the theoretical difficulties associated with the origination of conspicuous colouration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ratcliffe, John M -- Nydam, Marie L -- England -- Nature. 2008 Sep 4;455(7209):96-9. doi: 10.1038/nature07087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Sound Communication, Institute of Biology, University of Southern Denmark, DK-5230 Odense M, Denmark. jmr@biology.sdu.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18769439" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; Bayes Theorem ; Birds/*physiology ; Chiroptera/*physiology ; Circadian Rhythm ; Color ; Cues ; Molecular Sequence Data ; Moths/genetics/*physiology ; Ontario ; Phylogeny ; Pigmentation/*physiology ; Predatory Behavior/*physiology ; Seasons ; Ultrasonics
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    The Drosophila pheromone cVA activates a sexually dimorphic neural circuit (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-02-29
    Description: Courtship is an innate sexually dimorphic behaviour that can be observed in naive animals without previous learning or experience, suggesting that the neural circuits that mediate this behaviour are developmentally programmed. In Drosophila, courtship involves a complex yet stereotyped array of dimorphic behaviours that are regulated by Fru(M), a male-specific isoform of the fruitless gene. Fru(M) is expressed in about 2,000 neurons in the fly brain, including three subpopulations of olfactory sensory neurons and projection neurons (PNs). One set of Fru(+) olfactory neurons expresses the odorant receptor Or67d and responds to the male-specific pheromone cis-vaccenyl acetate (cVA). These neurons converge on the DA1 glomerulus in the antennal lobe. In males, activation of Or67d(+) neurons by cVA inhibits courtship of other males, whereas in females their activation promotes receptivity to other males. These observations pose the question of how a single pheromone acting through the same set of sensory neurons can elicit different behaviours in male and female flies. Anatomical or functional dimorphisms in this neural circuit might be responsible for the dimorphic behaviour. We therefore developed a neural tracing procedure that employs two-photon laser scanning microscopy to activate the photoactivatable green fluorescent protein. Here we show, using this technique, that the projections from the DA1 glomerulus to the protocerebrum are sexually dimorphic. We observe a male-specific axonal arbor in the lateral horn whose elaboration requires the expression of the transcription factor Fru(M) in DA1 projection neurons and other Fru(+) cells. The observation that cVA activates a sexually dimorphic circuit in the protocerebrum suggests a mechanism by which a single pheromone can elicit different behaviours in males and in females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Datta, Sandeep Robert -- Vasconcelos, Maria Luisa -- Ruta, Vanessa -- Luo, Sean -- Wong, Allan -- Demir, Ebru -- Flores, Jorge -- Balonze, Karen -- Dickson, Barry J -- Axel, Richard -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Mar 27;452(7186):473-7. doi: 10.1038/nature06808. Epub 2008 Feb 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics and Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18305480" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/*pharmacology ; Animals ; Courtship ; Drosophila/cytology/*drug effects/*physiology ; Drosophila Proteins/deficiency/genetics/metabolism ; Female ; Male ; Nerve Tissue Proteins/deficiency/genetics/metabolism ; Neural Pathways/*drug effects ; Neurons/drug effects/physiology ; Oleic Acids/*pharmacology ; Pheromones/*pharmacology ; Protein Isoforms/genetics/metabolism ; *Sex Characteristics ; Sexual Behavior, Animal/*drug effects/physiology ; Smell/drug effects/physiology ; Transcription Factors/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
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  • 3
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    Multi-genetic events collaboratively contribute to Pten-null leukaemia stem-cell formation (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-09
    Description: Cancer stem cells, which share many common properties and regulatory machineries with normal stem cells, have recently been proposed to be responsible for tumorigenesis and to contribute to cancer resistance. The main challenges in cancer biology are to identify cancer stem cells and to define the molecular events required for transforming normal cells to cancer stem cells. Here we show that Pten deletion in mouse haematopoietic stem cells leads to a myeloproliferative disorder, followed by acute T-lymphoblastic leukaemia (T-ALL). Self-renewable leukaemia stem cells (LSCs) are enriched in the c-Kit(mid)CD3(+)Lin(-) compartment, where unphosphorylated beta-catenin is significantly increased. Conditional ablation of one allele of the beta-catenin gene substantially decreases the incidence and delays the occurrence of T-ALL caused by Pten loss, indicating that activation of the beta-catenin pathway may contribute to the formation or expansion of the LSC population. Moreover, a recurring chromosomal translocation, T(14;15), results in aberrant overexpression of the c-myc oncogene in c-Kit(mid)CD3(+)Lin(-) LSCs and CD3(+) leukaemic blasts, recapitulating a subset of human T-ALL. No alterations in Notch1 signalling are detected in this model, suggesting that Pten inactivation and c-myc overexpression may substitute functionally for Notch1 abnormalities, leading to T-ALL development. Our study indicates that multiple genetic or molecular alterations contribute cooperatively to LSC transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840044/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840044/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Wei -- Lasky, Joseph L -- Chang, Chun-Ju -- Mosessian, Sherly -- Lewis, Xiaoman -- Xiao, Yun -- Yeh, Jennifer E -- Chen, James Y -- Iruela-Arispe, M Luisa -- Varella-Garcia, Marileila -- Wu, Hong -- CA16042/CA/NCI NIH HHS/ -- R01 CA121110/CA/NCI NIH HHS/ -- R01 CA121110-01A1/CA/NCI NIH HHS/ -- England -- Nature. 2008 May 22;453(7194):529-33. doi: 10.1038/nature06933. Epub 2008 May 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18463637" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/metabolism ; Cell Proliferation ; Chromosomes, Mammalian/genetics ; Female ; Hematopoietic Stem Cells/cytology/pathology ; In Situ Hybridization, Fluorescence ; Leukemia-Lymphoma, Adult T-Cell/*pathology ; Male ; Mice ; Neoplastic Stem Cells/*metabolism/*pathology ; PTEN Phosphohydrolase/*deficiency/*genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; Receptors, Antigen, T-Cell/genetics ; Translocation, Genetic ; beta Catenin/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-14
    Description: The autosomal dominant hyper-IgE syndrome (HIES, 'Job's syndrome') is characterized by recurrent and often severe pulmonary infections, pneumatoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and connective tissue. Mutations presumed to underlie HIES have recently been identified in stat3, the gene encoding STAT3 (signal transducer and activator of transcription 3) (refs 3, 4). Although impaired production of interferon-gamma and tumour-necrosis factor by T cells, diminished memory T-cell populations, decreased delayed-type-hypersensitivity responses and decreased in vitro lymphoproliferation in response to specific antigens have variably been described, specific immunological abnormalities that can explain the unique susceptibility to particular infections seen in HIES have not yet been defined. Here we show that interleukin (IL)-17 production by T cells is absent in HIES individuals. We observed that ex vivo T cells from subjects with HIES failed to produce IL-17, but not IL-2, tumour-necrosis factor or interferon-gamma, on mitogenic stimulation with staphylococcal enterotoxin B or on antigenic stimulation with Candida albicans or streptokinase. Purified naive T cells were unable to differentiate into IL-17-producing (T(H)17) T helper cells in vitro and had lower expression of retinoid-related orphan receptor (ROR)-gammat, which is consistent with a crucial role for STAT3 signalling in the generation of T(H)17 cells. T(H)17 cells have emerged as an important subset of helper T cells that are believed to be critical in the clearance of fungal and extracellular bacterial infections. Thus, our data suggest that the inability to produce T(H)17 cells is a mechanism underlying the susceptibility to the recurrent infections commonly seen in HIES.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864108/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milner, Joshua D -- Brenchley, Jason M -- Laurence, Arian -- Freeman, Alexandra F -- Hill, Brenna J -- Elias, Kevin M -- Kanno, Yuka -- Spalding, Christine -- Elloumi, Houda Z -- Paulson, Michelle L -- Davis, Joie -- Hsu, Amy -- Asher, Ava I -- O'Shea, John -- Holland, Steven M -- Paul, William E -- Douek, Daniel C -- Z99 AI999999/Intramural NIH HHS/ -- England -- Nature. 2008 Apr 10;452(7188):773-6. doi: 10.1038/nature06764. Epub 2008 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18337720" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Candida albicans/immunology ; *Cell Differentiation ; Child ; Child, Preschool ; Enterotoxins/immunology ; Female ; *Genes, Dominant ; Humans ; Interferon-gamma/biosynthesis/immunology ; Interleukin-17/*biosynthesis ; Interleukin-2/biosynthesis/immunology ; Job Syndrome/genetics/*immunology/metabolism/*pathology ; Male ; Middle Aged ; Streptokinase/metabolism ; T-Lymphocytes, Helper-Inducer/immunology/*metabolism/*pathology ; Tumor Necrosis Factor-alpha/biosynthesis/immunology
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  • 5
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    The draft genome of the transgenic tropical fruit tree papaya (Carica papaya Linnaeus) (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-25
    Description: Papaya, a fruit crop cultivated in tropical and subtropical regions, is known for its nutritional benefits and medicinal applications. Here we report a 3x draft genome sequence of 'SunUp' papaya, the first commercial virus-resistant transgenic fruit tree to be sequenced. The papaya genome is three times the size of the Arabidopsis genome, but contains fewer genes, including significantly fewer disease-resistance gene analogues. Comparison of the five sequenced genomes suggests a minimal angiosperm gene set of 13,311. A lack of recent genome duplication, atypical of other angiosperm genomes sequenced so far, may account for the smaller papaya gene number in most functional groups. Nonetheless, striking amplifications in gene number within particular functional groups suggest roles in the evolution of tree-like habit, deposition and remobilization of starch reserves, attraction of seed dispersal agents, and adaptation to tropical daylengths. Transgenesis at three locations is closely associated with chloroplast insertions into the nuclear genome, and with topoisomerase I recognition sites. Papaya offers numerous advantages as a system for fruit-tree functional genomics, and this draft genome sequence provides the foundation for revealing the basis of Carica's distinguishing morpho-physiological, medicinal and nutritional properties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836516/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836516/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ming, Ray -- Hou, Shaobin -- Feng, Yun -- Yu, Qingyi -- Dionne-Laporte, Alexandre -- Saw, Jimmy H -- Senin, Pavel -- Wang, Wei -- Ly, Benjamin V -- Lewis, Kanako L T -- Salzberg, Steven L -- Feng, Lu -- Jones, Meghan R -- Skelton, Rachel L -- Murray, Jan E -- Chen, Cuixia -- Qian, Wubin -- Shen, Junguo -- Du, Peng -- Eustice, Moriah -- Tong, Eric -- Tang, Haibao -- Lyons, Eric -- Paull, Robert E -- Michael, Todd P -- Wall, Kerr -- Rice, Danny W -- Albert, Henrik -- Wang, Ming-Li -- Zhu, Yun J -- Schatz, Michael -- Nagarajan, Niranjan -- Acob, Ricelle A -- Guan, Peizhu -- Blas, Andrea -- Wai, Ching Man -- Ackerman, Christine M -- Ren, Yan -- Liu, Chao -- Wang, Jianmei -- Wang, Jianping -- Na, Jong-Kuk -- Shakirov, Eugene V -- Haas, Brian -- Thimmapuram, Jyothi -- Nelson, David -- Wang, Xiyin -- Bowers, John E -- Gschwend, Andrea R -- Delcher, Arthur L -- Singh, Ratnesh -- Suzuki, Jon Y -- Tripathi, Savarni -- Neupane, Kabi -- Wei, Hairong -- Irikura, Beth -- Paidi, Maya -- Jiang, Ning -- Zhang, Wenli -- Presting, Gernot -- Windsor, Aaron -- Navajas-Perez, Rafael -- Torres, Manuel J -- Feltus, F Alex -- Porter, Brad -- Li, Yingjun -- Burroughs, A Max -- Luo, Ming-Cheng -- Liu, Lei -- Christopher, David A -- Mount, Stephen M -- Moore, Paul H -- Sugimura, Tak -- Jiang, Jiming -- Schuler, Mary A -- Friedman, Vikki -- Mitchell-Olds, Thomas -- Shippen, Dorothy E -- dePamphilis, Claude W -- Palmer, Jeffrey D -- Freeling, Michael -- Paterson, Andrew H -- Gonsalves, Dennis -- Wang, Lei -- Alam, Maqsudul -- R01 GM083873/GM/NIGMS NIH HHS/ -- R01 GM083873-05/GM/NIGMS NIH HHS/ -- R01 LM006845/LM/NLM NIH HHS/ -- R01 LM006845-08/LM/NLM NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):991-6. doi: 10.1038/nature06856.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hawaii Agriculture Research Center, Aiea, Hawaii 96701, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18432245" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics ; Carica/*genetics ; Contig Mapping ; Databases, Genetic ; Genes, Plant/genetics ; Genome, Plant/*genetics ; Molecular Sequence Data ; Plants, Genetically Modified/genetics ; Sequence Alignment ; Sequence Analysis, DNA ; Transcription Factors/genetics ; Tropical Climate
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  • 6
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    Somatic mutations affect key pathways in lung adenocarcinoma (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-25
    Description: Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Getz, Gad -- Wheeler, David A -- Mardis, Elaine R -- McLellan, Michael D -- Cibulskis, Kristian -- Sougnez, Carrie -- Greulich, Heidi -- Muzny, Donna M -- Morgan, Margaret B -- Fulton, Lucinda -- Fulton, Robert S -- Zhang, Qunyuan -- Wendl, Michael C -- Lawrence, Michael S -- Larson, David E -- Chen, Ken -- Dooling, David J -- Sabo, Aniko -- Hawes, Alicia C -- Shen, Hua -- Jhangiani, Shalini N -- Lewis, Lora R -- Hall, Otis -- Zhu, Yiming -- Mathew, Tittu -- Ren, Yanru -- Yao, Jiqiang -- Scherer, Steven E -- Clerc, Kerstin -- Metcalf, Ginger A -- Ng, Brian -- Milosavljevic, Aleksandar -- Gonzalez-Garay, Manuel L -- Osborne, John R -- Meyer, Rick -- Shi, Xiaoqi -- Tang, Yuzhu -- Koboldt, Daniel C -- Lin, Ling -- Abbott, Rachel -- Miner, Tracie L -- Pohl, Craig -- Fewell, Ginger -- Haipek, Carrie -- Schmidt, Heather -- Dunford-Shore, Brian H -- Kraja, Aldi -- Crosby, Seth D -- Sawyer, Christopher S -- Vickery, Tammi -- Sander, Sacha -- Robinson, Jody -- Winckler, Wendy -- Baldwin, Jennifer -- Chirieac, Lucian R -- Dutt, Amit -- Fennell, Tim -- Hanna, Megan -- Johnson, Bruce E -- Onofrio, Robert C -- Thomas, Roman K -- Tonon, Giovanni -- Weir, Barbara A -- Zhao, Xiaojun -- Ziaugra, Liuda -- Zody, Michael C -- Giordano, Thomas -- Orringer, Mark B -- Roth, Jack A -- Spitz, Margaret R -- Wistuba, Ignacio I -- Ozenberger, Bradley -- Good, Peter J -- Chang, Andrew C -- Beer, David G -- Watson, Mark A -- Ladanyi, Marc -- Broderick, Stephen -- Yoshizawa, Akihiko -- Travis, William D -- Pao, William -- Province, Michael A -- Weinstock, George M -- Varmus, Harold E -- Gabriel, Stacey B -- Lander, Eric S -- Gibbs, Richard A -- Meyerson, Matthew -- Wilson, Richard K -- P50 CA070907/CA/NCI NIH HHS/ -- R01 CA154365/CA/NCI NIH HHS/ -- U19 CA084953/CA/NCI NIH HHS/ -- U19 CA084953-050003/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1069-75. doi: 10.1038/nature07423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948947" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma, Bronchiolo-Alveolar/*genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung Neoplasms/*genetics ; Male ; Mutation/*genetics ; Proto-Oncogenes/genetics
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  • 7
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    Abundance and diversity of microbial life in ocean crust (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-30
    Description: Oceanic lithosphere exposed at the sea floor undergoes seawater-rock alteration reactions involving the oxidation and hydration of glassy basalt. Basalt alteration reactions are theoretically capable of supplying sufficient energy for chemolithoautotrophic growth. Such reactions have been shown to generate microbial biomass in the laboratory, but field-based support for the existence of microbes that are supported by basalt alteration is lacking. Here, using quantitative polymerase chain reaction, in situ hybridization and microscopy, we demonstrate that prokaryotic cell abundances on seafloor-exposed basalts are 3-4 orders of magnitude greater than in overlying deep sea water. Phylogenetic analyses of basaltic lavas from the East Pacific Rise (9 degrees N) and around Hawaii reveal that the basalt-hosted biosphere harbours high bacterial community richness and that community membership is shared between these sites. We hypothesize that alteration reactions fuel chemolithoautotrophic microorganisms, which constitute a trophic base of the basalt habitat, with important implications for deep-sea carbon cycling and chemical exchange between basalt and sea water.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santelli, Cara M -- Orcutt, Beth N -- Banning, Erin -- Bach, Wolfgang -- Moyer, Craig L -- Sogin, Mitchell L -- Staudigel, Hubert -- Edwards, Katrina J -- England -- Nature. 2008 May 29;453(7195):653-6. doi: 10.1038/nature06899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MIT/WHOI Joint Program in Oceanography and Ocean Engineering, Woods Hole Oceanographic Institution, Woods Hole, Massachusetts 02543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509444" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; Chemoautotrophic Growth ; Genes, Bacterial/genetics ; Geologic Sediments/*microbiology ; Hawaii ; History, Ancient ; *Marine Biology ; Molecular Sequence Data ; Pacific Ocean ; Phylogeny ; Polymerase Chain Reaction ; RNA, Ribosomal, 16S/genetics ; Seawater/microbiology ; *Silicates/metabolism ; Water Microbiology
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  • 8
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    Genetics of gene expression and its effect on disease (2008)
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    Publication Date: 2008-03-18
    Description: Common human diseases result from the interplay of many genes and environmental factors. Therefore, a more integrative biology approach is needed to unravel the complexity and causes of such diseases. To elucidate the complexity of common human diseases such as obesity, we have analysed the expression of 23,720 transcripts in large population-based blood and adipose tissue cohorts comprehensively assessed for various phenotypes, including traits related to clinical obesity. In contrast to the blood expression profiles, we observed a marked correlation between gene expression in adipose tissue and obesity-related traits. Genome-wide linkage and association mapping revealed a highly significant genetic component to gene expression traits, including a strong genetic effect of proximal (cis) signals, with 50% of the cis signals overlapping between the two tissues profiled. Here we demonstrate an extensive transcriptional network constructed from the human adipose data that exhibits significant overlap with similar network modules constructed from mouse adipose data. A core network module in humans and mice was identified that is enriched for genes involved in the inflammatory and immune response and has been found to be causally associated to obesity-related traits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Emilsson, Valur -- Thorleifsson, Gudmar -- Zhang, Bin -- Leonardson, Amy S -- Zink, Florian -- Zhu, Jun -- Carlson, Sonia -- Helgason, Agnar -- Walters, G Bragi -- Gunnarsdottir, Steinunn -- Mouy, Magali -- Steinthorsdottir, Valgerdur -- Eiriksdottir, Gudrun H -- Bjornsdottir, Gyda -- Reynisdottir, Inga -- Gudbjartsson, Daniel -- Helgadottir, Anna -- Jonasdottir, Aslaug -- Jonasdottir, Adalbjorg -- Styrkarsdottir, Unnur -- Gretarsdottir, Solveig -- Magnusson, Kristinn P -- Stefansson, Hreinn -- Fossdal, Ragnheidur -- Kristjansson, Kristleifur -- Gislason, Hjortur G -- Stefansson, Tryggvi -- Leifsson, Bjorn G -- Thorsteinsdottir, Unnur -- Lamb, John R -- Gulcher, Jeffrey R -- Reitman, Marc L -- Kong, Augustine -- Schadt, Eric E -- Stefansson, Kari -- England -- Nature. 2008 Mar 27;452(7186):423-8. doi: 10.1038/nature06758. Epub 2008 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE genetics, 101 Reykjavik, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18344981" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Animals ; Blood/metabolism ; Body Mass Index ; Cohort Studies ; European Continental Ancestry Group/genetics ; Female ; *Gene Expression Profiling ; Gene Expression Regulation/*genetics ; Genome, Human ; Humans ; Iceland ; Lod Score ; Male ; Mice ; Middle Aged ; Obesity/*genetics ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Sample Size ; Waist-Hip Ratio
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Human metabolic phenotype diversity and its association with diet and blood pressure (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-22
    Description: Metabolic phenotypes are the products of interactions among a variety of factors-dietary, other lifestyle/environmental, gut microbial and genetic. We use a large-scale exploratory analytical approach to investigate metabolic phenotype variation across and within four human populations, based on 1H NMR spectroscopy. Metabolites discriminating across populations are then linked to data for individuals on blood pressure, a major risk factor for coronary heart disease and stroke (leading causes of mortality worldwide). We analyse spectra from two 24-hour urine specimens for each of 4,630 participants from the INTERMAP epidemiological study, involving 17 population samples aged 40-59 in China, Japan, UK and USA. We show that urinary metabolite excretion patterns for East Asian and western population samples, with contrasting diets, diet-related major risk factors, and coronary heart disease/stroke rates, are significantly differentiated (P 〈 10(-16)), as are Chinese/Japanese metabolic phenotypes, and subgroups with differences in dietary vegetable/animal protein and blood pressure. Among discriminatory metabolites, we quantify four and show association (P 〈 0.05 to P 〈 0.0001) of mean 24-hour urinary formate excretion with blood pressure in multiple regression analyses for individuals. Mean 24-hour urinary excretion of alanine (direct) and hippurate (inverse), reflecting diet and gut microbial activities, are also associated with blood pressure of individuals. Metabolic phenotyping applied to high-quality epidemiological data offers the potential to develop an area of aetiopathogenetic knowledge involving discovery of novel biomarkers related to cardiovascular disease risk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, Elaine -- Loo, Ruey Leng -- Stamler, Jeremiah -- Bictash, Magda -- Yap, Ivan K S -- Chan, Queenie -- Ebbels, Tim -- De Iorio, Maria -- Brown, Ian J -- Veselkov, Kirill A -- Daviglus, Martha L -- Kesteloot, Hugo -- Ueshima, Hirotsugu -- Zhao, Liancheng -- Nicholson, Jeremy K -- Elliott, Paul -- R01 HL084228/HL/NHLBI NIH HHS/ -- R01 HL50490/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 May 15;453(7193):396-400. doi: 10.1038/nature06882. Epub 2008 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomolecular Medicine, Division of Surgery, Oncology, Reproductive Biology and Anaesthetics (SORA), Faculty of Medicine, Imperial College London, South Kensington Campus, London SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18425110" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alanine/urine ; Animals ; Blood Pressure/*physiology ; Cardiovascular Diseases/metabolism ; China ; *Diet ; Dietary Proteins/pharmacology ; Female ; Great Britain ; Hippurates/urine ; Humans ; Intestines/microbiology ; Japan ; Magnetic Resonance Spectroscopy ; Male ; Metabolism/*physiology ; Middle Aged ; Phenotype ; Principal Component Analysis ; Time Factors ; United States ; Vegetables/chemistry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-25
    Description: African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4(+) T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4(+) T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872475/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872475/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keele, Brandon F -- Jones, James Holland -- Terio, Karen A -- Estes, Jacob D -- Rudicell, Rebecca S -- Wilson, Michael L -- Li, Yingying -- Learn, Gerald H -- Beasley, T Mark -- Schumacher-Stankey, Joann -- Wroblewski, Emily -- Mosser, Anna -- Raphael, Jane -- Kamenya, Shadrack -- Lonsdorf, Elizabeth V -- Travis, Dominic A -- Mlengeya, Titus -- Kinsel, Michael J -- Else, James G -- Silvestri, Guido -- Goodall, Jane -- Sharp, Paul M -- Shaw, George M -- Pusey, Anne E -- Hahn, Beatrice H -- HHSN266200400088C/PHS HHS/ -- P30 AI 27767/AI/NIAID NIH HHS/ -- P30 AI027767/AI/NIAID NIH HHS/ -- P30 AI027767-21A17134/AI/NIAID NIH HHS/ -- R01 AI058715/AI/NIAID NIH HHS/ -- R01 AI058715-06A1/AI/NIAID NIH HHS/ -- R01 AI50529/AI/NIAID NIH HHS/ -- R01 AI58715/AI/NIAID NIH HHS/ -- R37 AI050529/AI/NIAID NIH HHS/ -- R37 AI050529-06A1/AI/NIAID NIH HHS/ -- RR-00165/RR/NCRR NIH HHS/ -- T32 GM008111/GM/NIGMS NIH HHS/ -- U19 AI067854/AI/NIAID NIH HHS/ -- U19 AI067854-059010/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 23;460(7254):515-9. doi: 10.1038/nature08200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626114" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/pathology ; Africa ; Animals ; Animals, Wild ; CD4-Positive T-Lymphocytes/immunology ; Female ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/*virology ; Prevalence ; Simian Acquired Immunodeficiency ; Syndrome/epidemiology/immunology/*mortality/*pathology ; Simian Immunodeficiency Virus/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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