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  • 1
    Publication Date: 2016-03-17
    Description: Microbial viruses can control host abundances via density-dependent lytic predator-prey dynamics. Less clear is how temperate viruses, which coexist and replicate with their host, influence microbial communities. Here we show that virus-like particles are relatively less abundant at high host densities. This suggests suppressed lysis where established models predict lytic dynamics are favoured. Meta-analysis of published viral and microbial densities showed that this trend was widespread in diverse ecosystems ranging from soil to freshwater to human lungs. Experimental manipulations showed viral densities more consistent with temperate than lytic life cycles at increasing microbial abundance. An analysis of 24 coral reef viromes showed a relative increase in the abundance of hallmark genes encoded by temperate viruses with increased microbial abundance. Based on these four lines of evidence, we propose the Piggyback-the-Winner model wherein temperate dynamics become increasingly important in ecosystems with high microbial densities; thus 'more microbes, fewer viruses'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knowles, B -- Silveira, C B -- Bailey, B A -- Barott, K -- Cantu, V A -- Cobian-Guemes, A G -- Coutinho, F H -- Dinsdale, E A -- Felts, B -- Furby, K A -- George, E E -- Green, K T -- Gregoracci, G B -- Haas, A F -- Haggerty, J M -- Hester, E R -- Hisakawa, N -- Kelly, L W -- Lim, Y W -- Little, M -- Luque, A -- McDole-Somera, T -- McNair, K -- de Oliveira, L S -- Quistad, S D -- Robinett, N L -- Sala, E -- Salamon, P -- Sanchez, S E -- Sandin, S -- Silva, G G Z -- Smith, J -- Sullivan, C -- Thompson, C -- Vermeij, M J A -- Youle, M -- Young, C -- Zgliczynski, B -- Brainard, R -- Edwards, R A -- Nulton, J -- Thompson, F -- Rohwer, F -- England -- Nature. 2016 Mar 24;531(7595):466-70. doi: 10.1038/nature17193. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Biology Institute, Rio de Janeiro Federal University, Av. Carlos Chagas Filho 373, Rio de Janeiro, Rio de Janeiro 21941-599, Brazil. ; Department of Mathematics and Statistics, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Hawaii Institute of Marine Biology, University of Hawaii at Manoa, 46-007 Lilipuna Road, Kaneohe, Hawaii 96744, USA. ; Computational Science Research Center, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Rainbow Rock, Ocean View, Hawaii 96737, USA. ; Radboud University Medical Centre, Radboud Institute for Molecular Life Sciences, Centre for Molecular and Biomolecular Informatics, 6525HP Nijmegen, The Netherlands. ; Viral Information Institute, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Scripps Institution of Oceanography, 8622 Kennel Way, La Jolla, California 92037, USA. ; Department of Biology, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Marine Sciences Department, Sao Paulo Federal University - Baixada Santista, Av. Alm. Saldanha da Gama, 89, Santos, Sao Paulo 11030-400, Brazil. ; National Geographic Society, 1145 17th St NW, Washington D.C. 20036, USA. ; CARMABI Foundation, Piscaderabaai z/n, Willemstad, Curacao, Netherlands Antilles. ; Aquatic Microbiology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, 1098XH Amsterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/physiology/*virology ; Bacteriophages/pathogenicity/physiology ; Coral Reefs ; *Ecosystem ; Genes, Viral/genetics ; *Host-Pathogen Interactions ; Lysogeny ; Models, Biological ; Virulence/genetics ; Viruses/genetics/isolation & purification/*pathogenicity
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  • 2
    Publication Date: 2012-11-20
    Description: The prefrontal cortex (PFC) is thought to participate in high-level control of the generation of behaviours (including the decision to execute actions); indeed, imaging and lesion studies in human beings have revealed that PFC dysfunction can lead to either impulsive states with increased tendency to initiate action, or to amotivational states characterized by symptoms such as reduced activity, hopelessness and depressed mood. Considering the opposite valence of these two phenotypes as well as the broad complexity of other tasks attributed to PFC, we sought to elucidate the PFC circuitry that favours effortful behavioural responses to challenging situations. Here we develop and use a quantitative method for the continuous assessment and control of active response to a behavioural challenge, synchronized with single-unit electrophysiology and optogenetics in freely moving rats. In recording from the medial PFC (mPFC), we observed that many neurons were not simply movement-related in their spike-firing patterns but instead were selectively modulated from moment to moment, according to the animal's decision to act in a challenging situation. Surprisingly, we next found that direct activation of principal neurons in the mPFC had no detectable causal effect on this behaviour. We tested whether this behaviour could be causally mediated by only a subclass of mPFC cells defined by specific downstream wiring. Indeed, by leveraging optogenetic projection-targeting to control cells with specific efferent wiring patterns, we found that selective activation of those mPFC cells projecting to the brainstem dorsal raphe nucleus (DRN), a serotonergic nucleus implicated in major depressive disorder, induced a profound, rapid and reversible effect on selection of the active behavioural state. These results may be of importance in understanding the neural circuitry underlying normal and pathological patterns of action selection and motivation in behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warden, Melissa R -- Selimbeyoglu, Aslihan -- Mirzabekov, Julie J -- Lo, Maisie -- Thompson, Kimberly R -- Kim, Sung-Yon -- Adhikari, Avishek -- Tye, Kay M -- Frank, Loren M -- Deisseroth, Karl -- 1F32MH088010-01/MH/NIMH NIH HHS/ -- F32 MH088010/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 20;492(7429):428-32. doi: 10.1038/nature11617.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, California 94305, USA. mwarden@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23160494" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Behavior, Animal/*physiology ; Depression/psychology ; Electrophysiology ; Locomotion/physiology ; Male ; Motivation/*physiology ; Neurons/*physiology ; Optogenetics ; Prefrontal Cortex/*physiology ; Raphe Nuclei/*physiology ; Rats ; Rats, Long-Evans ; Swimming/*physiology ; Synapses/physiology ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2012-02-07
    Description: Dynamic variations in the structure of chromatin influence virtually all DNA-related processes in eukaryotes and are controlled in part by post-translational modifications of histones. One such modification, the acetylation of lysine 56 (H3K56ac) in the amino-terminal alpha-helix (alphaN) of histone H3, has been implicated in the regulation of nucleosome assembly during DNA replication and repair, and nucleosome disassembly during gene transcription. In Saccharomyces cerevisiae, the histone chaperone Rtt106 contributes to the deposition of newly synthesized H3K56ac-carrying H3-H4 complex on replicating DNA, but it is unclear how Rtt106 binds H3-H4 and specifically recognizes H3K56ac as there is no apparent acetylated lysine reader domain in Rtt106. Here, we show that two domains of Rtt106 are involved in a combinatorial recognition of H3-H4. An N-terminal domain homodimerizes and interacts with H3-H4 independently of acetylation while a double pleckstrin-homology (PH) domain binds the K56-containing region of H3. Affinity is markedly enhanced upon acetylation of K56, an effect that is probably due to increased conformational entropy of the alphaN helix of H3. Our data support a mode of interaction where the N-terminal homodimeric domain of Rtt106 intercalates between the two H3-H4 components of the (H3-H4)(2) tetramer while two double PH domains in the Rtt106 dimer interact with each of the two H3K56ac sites in (H3-H4)(2). We show that the Rtt106-(H3-H4)(2) interaction is important for gene silencing and the DNA damage response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439842/" 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/PMC3439842/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Dan -- Hu, Qi -- Li, Qing -- Thompson, James R -- Cui, Gaofeng -- Fazly, Ahmed -- Davies, Brian A -- Botuyan, Maria Victoria -- Zhang, Zhiguo -- Mer, Georges -- P50 CA108961/CA/NCI NIH HHS/ -- R01 CA132878/CA/NCI NIH HHS/ -- R01 CA132878-04/CA/NCI NIH HHS/ -- R01 GM072719/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Feb 5;483(7387):104-7. doi: 10.1038/nature10861.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22307274" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Binding Sites ; Crystallography, X-Ray ; DNA Damage ; Gene Silencing ; Genomic Instability ; Histones/*chemistry/*metabolism ; Lysine/analogs & derivatives/chemistry/metabolism ; Magnetic Resonance Spectroscopy ; Models, Molecular ; Molecular Chaperones/*chemistry/genetics/*metabolism ; Mutation/genetics ; Pliability ; Protein Binding ; Protein Multimerization ; Protein Structure, Tertiary ; Saccharomyces cerevisiae/*chemistry ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Structure-Activity Relationship ; Substrate Specificity ; Xenopus laevis
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Helen -- England -- Nature. 2012 May 29;485(7400):556-7. doi: 10.1038/485556a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Confidentiality ; *Environment ; Environmental Exposure/*adverse effects/legislation & jurisprudence ; Environmental Monitoring ; Extraction and Processing Industry/economics/*legislation & jurisprudence ; Female ; Humans ; Livestock ; Ohio ; *Oil and Gas Fields ; Pregnancy ; *Public Health/legislation & jurisprudence ; Sentinel Surveillance ; United States ; United States Environmental Protection Agency
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Picha, Brad -- Thompson, Matthew -- Vondriska, Thomas M -- England -- Nature. 2012 May 2;485(7396):41. doi: 10.1038/485041d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22552083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*standards ; Drug Evaluation, Preclinical/*standards ; Humans ; Neoplasms/*drug therapy ; Translational Medical Research/*statistics & numerical data
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  • 6
    Publication Date: 2013-06-07
    Description: Previous investigations of the core gene regulatory circuitry that controls the pluripotency of embryonic stem (ES) cells have largely focused on the roles of transcription, chromatin and non-coding RNA regulators. Alternative splicing represents a widely acting mode of gene regulation, yet its role in regulating ES-cell pluripotency and differentiation is poorly understood. Here we identify the muscleblind-like RNA binding proteins, MBNL1 and MBNL2, as conserved and direct negative regulators of a large program of cassette exon alternative splicing events that are differentially regulated between ES cells and other cell types. Knockdown of MBNL proteins in differentiated cells causes switching to an ES-cell-like alternative splicing pattern for approximately half of these events, whereas overexpression of MBNL proteins in ES cells promotes differentiated-cell-like alternative splicing patterns. Among the MBNL-regulated events is an ES-cell-specific alternative splicing switch in the forkhead family transcription factor FOXP1 that controls pluripotency. Consistent with a central and negative regulatory role for MBNL proteins in pluripotency, their knockdown significantly enhances the expression of key pluripotency genes and the formation of induced pluripotent stem cells during somatic cell reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933998/" 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/PMC3933998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Hong -- Irimia, Manuel -- Ross, P Joel -- Sung, Hoon-Ki -- Alipanahi, Babak -- David, Laurent -- Golipour, Azadeh -- Gabut, Mathieu -- Michael, Iacovos P -- Nachman, Emil N -- Wang, Eric -- Trcka, Dan -- Thompson, Tadeo -- O'Hanlon, Dave -- Slobodeniuc, Valentina -- Barbosa-Morais, Nuno L -- Burge, Christopher B -- Moffat, Jason -- Frey, Brendan J -- Nagy, Andras -- Ellis, James -- Wrana, Jeffrey L -- Blencowe, Benjamin J -- R01 HG002439/HG/NHGRI NIH HHS/ -- R33 MH087908/MH/NIMH NIH HHS/ -- R33MH087908/MH/NIMH NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Jun 13;498(7453):241-5. doi: 10.1038/nature12270. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research and Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739326" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing/genetics ; Amino Acid Motifs ; Animals ; Cell Differentiation/genetics ; Cell Line ; *Cellular Reprogramming ; DNA-Binding Proteins/chemistry/deficiency/genetics/*metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Fibroblasts/cytology/metabolism ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; HeLa Cells ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Kinetics ; Mice ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Repressor Proteins/metabolism
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  • 7
    Publication Date: 2013-02-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rochman, Chelsea M -- Browne, Mark Anthony -- Halpern, Benjamin S -- Hentschel, Brian T -- Hoh, Eunha -- Karapanagioti, Hrissi K -- Rios-Mendoza, Lorena M -- Takada, Hideshige -- Teh, Swee -- Thompson, Richard C -- England -- Nature. 2013 Feb 14;494(7436):169-71. doi: 10.1038/494169a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Veterinary Medicine, University of California, Davis, USA. cmrochman@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23407523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Environmental Monitoring ; *Environmental Policy/economics ; Hazardous Waste/*adverse effects/analysis/classification/*prevention & control ; Humans ; Plastics/*adverse effects/analysis/chemistry/*classification ; Recycling/trends ; Refuse Disposal/economics/*legislation & jurisprudence/*statistics & numerical ; data
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2012-12-14
    Description: Major depression is characterized by diverse debilitating symptoms that include hopelessness and anhedonia. Dopamine neurons involved in reward and motivation are among many neural populations that have been hypothesized to be relevant, and certain antidepressant treatments, including medications and brain stimulation therapies, can influence the complex dopamine system. Until now it has not been possible to test this hypothesis directly, even in animal models, as existing therapeutic interventions are unable to specifically target dopamine neurons. Here we investigated directly the causal contributions of defined dopamine neurons to multidimensional depression-like phenotypes induced by chronic mild stress, by integrating behavioural, pharmacological, optogenetic and electrophysiological methods in freely moving rodents. We found that bidirectional control (inhibition or excitation) of specified midbrain dopamine neurons immediately and bidirectionally modulates (induces or relieves) multiple independent depression symptoms caused by chronic stress. By probing the circuit implementation of these effects, we observed that optogenetic recruitment of these dopamine neurons potently alters the neural encoding of depression-related behaviours in the downstream nucleus accumbens of freely moving rodents, suggesting that processes affecting depression symptoms may involve alterations in the neural encoding of action in limbic circuitry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160519/" 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/PMC4160519/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tye, Kay M -- Mirzabekov, Julie J -- Warden, Melissa R -- Ferenczi, Emily A -- Tsai, Hsing-Chen -- Finkelstein, Joel -- Kim, Sung-Yon -- Adhikari, Avishek -- Thompson, Kimberly R -- Andalman, Aaron S -- Gunaydin, Lisa A -- Witten, Ilana B -- Deisseroth, Karl -- DP2 DA035149/DA/NIDA NIH HHS/ -- F32 MH880102/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jan 24;493(7433):537-41. doi: 10.1038/nature11740. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. kaytye@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Depression/chemically induced/*physiopathology ; Dopamine/metabolism ; Dopaminergic Neurons/drug effects/*metabolism/radiation effects ; Female ; Male ; Mice ; Models, Neurological ; Nucleus Accumbens/metabolism ; Optogenetics ; Phenotype ; Rats ; Rats, Long-Evans ; Stress, Psychological/physiopathology ; Time Factors ; Ventral Tegmental Area/cytology
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  • 9
    Publication Date: 2014-05-09
    Description: ATP is the dominant energy source in animals for mechanical and electrical work (for example, muscle contraction or neuronal firing). For chemical work, there is an equally important role for NADPH, which powers redox defence and reductive biosynthesis. The most direct route to produce NADPH from glucose is the oxidative pentose phosphate pathway, with malic enzyme sometimes also important. Although the relative contribution of glycolysis and oxidative phosphorylation to ATP production has been extensively analysed, similar analysis of NADPH metabolism has been lacking. Here we demonstrate the ability to directly track, by liquid chromatography-mass spectrometry, the passage of deuterium from labelled substrates into NADPH, and combine this approach with carbon labelling and mathematical modelling to measure NADPH fluxes. In proliferating cells, the largest contributor to cytosolic NADPH is the oxidative pentose phosphate pathway. Surprisingly, a nearly comparable contribution comes from serine-driven one-carbon metabolism, in which oxidation of methylene tetrahydrofolate to 10-formyl-tetrahydrofolate is coupled to reduction of NADP(+) to NADPH. Moreover, tracing of mitochondrial one-carbon metabolism revealed complete oxidation of 10-formyl-tetrahydrofolate to make NADPH. As folate metabolism has not previously been considered an NADPH producer, confirmation of its functional significance was undertaken through knockdown of methylenetetrahydrofolate dehydrogenase (MTHFD) genes. Depletion of either the cytosolic or mitochondrial MTHFD isozyme resulted in decreased cellular NADPH/NADP(+) and reduced/oxidized glutathione ratios (GSH/GSSG) and increased cell sensitivity to oxidative stress. Thus, although the importance of folate metabolism for proliferating cells has been long recognized and attributed to its function of producing one-carbon units for nucleic acid synthesis, another crucial function of this pathway is generating reducing power.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104482/" 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/PMC4104482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Jing -- Ye, Jiangbin -- Kamphorst, Jurre J -- Shlomi, Tomer -- Thompson, Craig B -- Rabinowitz, Joshua D -- P01 CA104838/CA/NCI NIH HHS/ -- P30 CA072720/CA/NCI NIH HHS/ -- P50 GM071508/GM/NIGMS NIH HHS/ -- R01 AI097382/AI/NIAID NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- R01 CA163591/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jun 12;510(7504):298-302. doi: 10.1038/nature13236. Epub 2014 May 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA [2]. ; 1] Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2]. ; Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA. ; 1] Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA [2] Department of Computer Science, Technion - Israel Institute of Technology, Haifa 32000, Israel. ; Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24805240" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon/metabolism ; Cell Line ; Cell Line, Tumor ; Cytosol/enzymology/metabolism ; Folic Acid/*metabolism ; Glutathione/metabolism ; Glycine/metabolism ; HEK293 Cells ; Humans ; Isoenzymes/deficiency/genetics/metabolism ; Leucovorin/analogs & derivatives/metabolism ; Methylenetetrahydrofolate Dehydrogenase (NADP)/deficiency/genetics/metabolism ; Mice ; Mitochondria/enzymology/metabolism ; NADP/*biosynthesis/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Pentose Phosphate Pathway ; Serine/metabolism ; Tetrahydrofolates/metabolism
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  • 10
    Publication Date: 2014-08-29
    Description: The transcriptome is the readout of the genome. Identifying common features in it across distant species can reveal fundamental principles. To this end, the ENCODE and modENCODE consortia have generated large amounts of matched RNA-sequencing data for human, worm and fly. Uniform processing and comprehensive annotation of these data allow comparison across metazoan phyla, extending beyond earlier within-phylum transcriptome comparisons and revealing ancient, conserved features. Specifically, we discover co-expression modules shared across animals, many of which are enriched in developmental genes. Moreover, we use expression patterns to align the stages in worm and fly development and find a novel pairing between worm embryo and fly pupae, in addition to the embryo-to-embryo and larvae-to-larvae pairings. Furthermore, we find that the extent of non-canonical, non-coding transcription is similar in each organism, per base pair. Finally, we find in all three organisms that the gene-expression levels, both coding and non-coding, can be quantitatively predicted from chromatin features at the promoter using a 'universal model' based on a single set of organism-independent parameters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155737/" 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/PMC4155737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerstein, Mark B -- Rozowsky, Joel -- Yan, Koon-Kiu -- Wang, Daifeng -- Cheng, Chao -- Brown, James B -- Davis, Carrie A -- Hillier, LaDeana -- Sisu, Cristina -- Li, Jingyi Jessica -- Pei, Baikang -- Harmanci, Arif O -- Duff, Michael O -- Djebali, Sarah -- Alexander, Roger P -- Alver, Burak H -- Auerbach, Raymond -- Bell, Kimberly -- Bickel, Peter J -- Boeck, Max E -- Boley, Nathan P -- Booth, Benjamin W -- Cherbas, Lucy -- Cherbas, Peter -- Di, Chao -- Dobin, Alex -- Drenkow, Jorg -- Ewing, Brent -- Fang, Gang -- Fastuca, Megan -- Feingold, Elise A -- Frankish, Adam -- Gao, Guanjun -- Good, Peter J -- Guigo, Roderic -- Hammonds, Ann -- Harrow, Jen -- Hoskins, Roger A -- Howald, Cedric -- Hu, Long -- Huang, Haiyan -- Hubbard, Tim J P -- Huynh, Chau -- Jha, Sonali -- Kasper, Dionna -- Kato, Masaomi -- Kaufman, Thomas C -- Kitchen, Robert R -- Ladewig, Erik -- Lagarde, Julien -- Lai, Eric -- Leng, Jing -- Lu, Zhi -- MacCoss, Michael -- May, Gemma -- McWhirter, Rebecca -- Merrihew, Gennifer -- Miller, David M -- Mortazavi, Ali -- Murad, Rabi -- Oliver, Brian -- Olson, Sara -- Park, Peter J -- Pazin, Michael J -- Perrimon, Norbert -- Pervouchine, Dmitri -- Reinke, Valerie -- Reymond, Alexandre -- Robinson, Garrett -- Samsonova, Anastasia -- Saunders, Gary I -- Schlesinger, Felix -- Sethi, Anurag -- Slack, Frank J -- Spencer, William C -- Stoiber, Marcus H -- Strasbourger, Pnina -- Tanzer, Andrea -- Thompson, Owen A -- Wan, Kenneth H -- Wang, Guilin -- Wang, Huaien -- Watkins, Kathie L -- Wen, Jiayu -- Wen, Kejia -- Xue, Chenghai -- Yang, Li -- Yip, Kevin -- Zaleski, Chris -- Zhang, Yan -- Zheng, Henry -- Brenner, Steven E -- Graveley, Brenton R -- Celniker, Susan E -- Gingeras, Thomas R -- Waterston, Robert -- 1U01HG007031-01/HG/NHGRI NIH HHS/ -- 5U01HG004695-04/HG/NHGRI NIH HHS/ -- 5U54HG004555/HG/NHGRI NIH HHS/ -- HG007000/HG/NHGRI NIH HHS/ -- HG007355/HG/NHGRI NIH HHS/ -- K99 HG006698/HG/NHGRI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 GM076655/GM/NIGMS NIH HHS/ -- RC2-HG005639/HG/NHGRI NIH HHS/ -- T15 LM007056/LM/NLM NIH HHS/ -- T32 HD060555/HD/NICHD NIH HHS/ -- U01 HG 004263/HG/NHGRI NIH HHS/ -- U01 HG004261/HG/NHGRI NIH HHS/ -- U01 HG004271/HG/NHGRI NIH HHS/ -- U01 HG007031/HG/NHGRI NIH HHS/ -- U01-HG004261/HG/NHGRI NIH HHS/ -- U01HG004258/HG/NHGRI NIH HHS/ -- U41 HG007000/HG/NHGRI NIH HHS/ -- U41 HG007234/HG/NHGRI NIH HHS/ -- U41 HG007355/HG/NHGRI NIH HHS/ -- U54 HG004555/HG/NHGRI NIH HHS/ -- U54 HG006944/HG/NHGRI NIH HHS/ -- U54 HG006994/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- U54 HG007005/HG/NHGRI NIH HHS/ -- U54HG007005/HG/NHGRI NIH HHS/ -- WT098051/Wellcome Trust/United Kingdom -- ZIA DK015600-18/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 28;512(7515):445-8. doi: 10.1038/nature13424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [3] Department of Computer Science, Yale University, 51 Prospect Street, New Haven, Connecticut 06511, USA [4] [5]. ; 1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [3]. ; 1] Department of Genetics, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, USA [2] Institute for Quantitative Biomedical Sciences, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire 03766, USA [3]. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2] Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA [3]. ; 1] Functional Genomics, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA [2]. ; 1] Department of Genome Sciences and University of Washington School of Medicine, William H. Foege Building S350D, 1705 Northeast Pacific Street, Box 355065 Seattle, Washington 98195-5065, USA [2]. ; 1] Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA [2] Department of Statistics, University of California, Los Angeles, California 90095-1554, USA [3] Department of Human Genetics, University of California, Los Angeles, California 90095-7088, USA [4]. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2]. ; 1] Centre for Genomic Regulation, Doctor Aiguader 88, 08003 Barcelona, Catalonia, Spain [2] Departament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Catalonia, Spain [3]. ; 1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA. ; Center for Biomedical Informatics, Harvard Medical School, 10 Shattuck Street, Boston, Massachusetts 02115, USA. ; Functional Genomics, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. ; Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA. ; Department of Genome Sciences and University of Washington School of Medicine, William H. Foege Building S350D, 1705 Northeast Pacific Street, Box 355065 Seattle, Washington 98195-5065, USA. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2] Department of Biostatistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA. ; Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. ; 1] Department of Biology, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA [2] Center for Genomics and Bioinformatics, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA. ; MOE Key Lab of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China. ; National Human Genome Research Institute, National Institutes of Health, 5635 Fishers Lane, Bethesda, Maryland 20892-9307, USA. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. ; 1] Centre for Genomic Regulation, Doctor Aiguader 88, 08003 Barcelona, Catalonia, Spain [2] Departament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Catalonia, Spain. ; 1] Center for Integrative Genomics, University of Lausanne, Genopode building, Lausanne 1015, Switzerland [2] Swiss Institute of Bioinformatics, Genopode building, Lausanne 1015, Switzerland. ; 1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK [2] Medical and Molecular Genetics, King's College London, London WC2R 2LS, UK. ; Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06520-8005, USA. ; Department of Molecular, Cellular and Developmental Biology, PO Box 208103, Yale University, New Haven, Connecticut 06520, USA. ; Department of Biology, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA. ; Sloan-Kettering Institute, 1275 York Avenue, Box 252, New York, New York 10065, USA. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2] Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213 USA. ; Department of Cell and Developmental Biology, Vanderbilt University, 465 21st Avenue South, Nashville, Tennessee 37232-8240, USA. ; 1] Developmental and Cell Biology, University of California, Irvine, California 92697, USA [2] Center for Complex Biological Systems, University of California, Irvine, California 92697, USA. ; Section of Developmental Genomics, Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA. ; 1] Department of Genetics and Drosophila RNAi Screening Center, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA [2] Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. ; Center for Integrative Genomics, University of Lausanne, Genopode building, Lausanne 1015, Switzerland. ; 1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK [2] European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SD, UK. ; 1] Bioinformatics and Genomics Programme, Center for Genomic Regulation, Universitat Pompeu Fabra (CRG-UPF), 08003 Barcelona, Catalonia, Spain [2] Institute for Theoretical Chemistry, Theoretical Biochemistry Group (TBI), University of Vienna, Wahringerstrasse 17/3/303, A-1090 Vienna, Austria. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2] Key Laboratory of Computational Biology, CAS-MPG Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; 1] Hong Kong Bioinformatics Centre, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong [2] 5 CUHK-BGI Innovation Institute of Trans-omics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. ; 1] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA [2] Department of Plant and Microbial Biology, University of California, Berkeley, California 94720, USA [3]. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25164755" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/growth & development ; Chromatin/genetics ; Cluster Analysis ; Drosophila melanogaster/*genetics/growth & development ; *Gene Expression Profiling ; Gene Expression Regulation, Developmental/genetics ; Histones/metabolism ; Humans ; Larva/genetics/growth & development ; Models, Genetic ; Molecular Sequence Annotation ; Promoter Regions, Genetic/genetics ; Pupa/genetics/growth & development ; RNA, Untranslated/genetics ; Sequence Analysis, RNA ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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