ALBERT

Description: Telomeres cap the ends of chromosomes and provide a means to complete replication. The DNA portion of telomeres is synthesized by the enzyme telomerase using part of an RNA subunit as a template for reverse transcription. How the mature 3' end of telomerase RNA is generated has so far remained elusive. Here we show that in Schizosaccharomyces pombe telomerase RNA transcripts must be processed to generate functional telomerase. Characterization of the maturation pathway uncovered an unexpected role for the spliceosome, which normally catalyses splicing of pre-messenger RNA. The first spliceosomal cleavage reaction generates the mature 3' end of telomerase RNA (TER1, the functional RNA encoded by the ter1(+) gene), releasing the active form of the RNA without exon ligation. Blocking the first step or permitting completion of splicing generates inactive forms of TER1 and causes progressive telomere shortening. We establish that 3' end processing of TER1 is critical for telomerase function and describe a previously unknown mechanism for RNA maturation that uses the ability of the spliceosome to mediate site-specific cleavage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Box, Jessica A -- Bunch, Jeremy T -- Tang, Wen -- Baumann, Peter -- England -- Nature. 2008 Dec 18;456(7224):910-4. doi: 10.1038/nature07584. Epub 2008 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19052544" target="_blank"〉PubMed〈/a〉

Description: Most molecular clouds are filamentary or elongated. For those forming low-mass stars (〈8 solar masses), the competition between self-gravity and turbulent pressure along the dynamically dominant intercloud magnetic field (10 to 100 parsecs) shapes the clouds to be elongated either perpendicularly or parallel to the fields. A recent study also suggested that on the scales of 0.1 to 0.01 parsecs, such fields are dynamically important within cloud cores forming massive stars (〉8 solar masses). But whether the core field morphologies are inherited from the intercloud medium or governed by cloud turbulence is unknown, as is the effect of magnetic fields on cloud fragmentation at scales of 10 to 0.1 parsecs. Here we report magnetic-field maps inferred from polarimetric observations of NGC 6334, a region forming massive stars, on the 100 to 0.01 parsec scale. NGC 6334 hosts young star-forming sites where fields are not severely affected by stellar feedback, and their directions do not change much over the entire scale range. This means that the fields are dynamically important. The ordered fields lead to a self-similar gas fragmentation: at all scales, there exist elongated gas structures nearly perpendicular to the fields. Many gas elongations have density peaks near the ends, which symmetrically pinch the fields. The field strength is proportional to the 0.4th power of the density, which is an indication of anisotropic gas contractions along the field. We conclude that magnetic fields have a crucial role in the fragmentation of NGC 6334.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hua-bai -- Yuen, Ka Ho -- Otto, Frank -- Leung, Po Kin -- Sridharan, T K -- Zhang, Qizhou -- Liu, Hauyu -- Tang, Ya-Wen -- Qiu, Keping -- England -- Nature. 2015 Apr 23;520(7548):518-21. doi: 10.1038/nature14291. Epub 2015 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, The Chinese University of Hong Kong, Shatin, New Territory, Hong Kong, China. ; Harvard-Smithsonian Center for Astrophysics, 60 Garden Street, Cambridge, Massachusetts 02138, USA. ; Academia Sinica Institute of Astronomy and Astrophysics, 11F Astronomy-Mathematics Building, AS/NTU (National Taiwan University) No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan, China. ; School of Astronomy and Space Science, Nanjing University, 22 Hankou Road, Nanjing, Jiangsu 210093, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25822792" target="_blank"〉PubMed〈/a〉

Description: In most eukaryotes, the progressive loss of chromosome-terminal DNA sequences is counteracted by the enzyme telomerase, a reverse transcriptase that uses part of an RNA subunit as template to synthesize telomeric repeats. Many cancer cells express high telomerase activity, and mutations in telomerase subunits are associated with degenerative syndromes including dyskeratosis congenita and aplastic anaemia. The therapeutic value of altering telomerase activity thus provides ample impetus to study the biogenesis and regulation of this enzyme in human cells and model systems. We have previously identified a precursor of the fission yeast telomerase RNA subunit (TER1) and demonstrated that the mature 3'-end is generated by the spliceosome in a single cleavage reaction akin to the first step of splicing. Directly upstream and partly overlapping with the spliceosomal cleavage site is a putative binding site for Sm proteins. Sm and like-Sm (LSm) proteins belong to an ancient family of RNA-binding proteins represented in all three domains of life. Members of this family form ring complexes on specific sets of target RNAs and have critical roles in their biogenesis, function and turnover. Here we demonstrate that the canonical Sm ring and the Lsm2-8 complex sequentially associate with fission yeast TER1. The Sm ring binds to the TER1 precursor, stimulates spliceosomal cleavage and promotes the hypermethylation of the 5'-cap by Tgs1. Sm proteins are then replaced by the Lsm2-8 complex, which promotes the association with the catalytic subunit and protects the mature 3'-end of TER1 from exonucleolytic degradation. Our findings define the sequence of events that occur during telomerase biogenesis and characterize roles for Sm and Lsm complexes as well as for the methylase Tgs1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326189/" 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/PMC3326189/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wen -- Kannan, Ram -- Blanchette, Marco -- Baumann, Peter -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 25;484(7393):260-4. doi: 10.1038/nature10924.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Kansas City, Missouri 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22446625" target="_blank"〉PubMed〈/a〉

Description: Platelets are the second most abundant cell type in blood and are essential for maintaining haemostasis. Their count and volume are tightly controlled within narrow physiological ranges, but there is only limited understanding of the molecular processes controlling both traits. Here we carried out a high-powered meta-analysis of genome-wide association studies (GWAS) in up to 66,867 individuals of European ancestry, followed by extensive biological and functional assessment. We identified 68 genomic loci reliably associated with platelet count and volume mapping to established and putative novel regulators of megakaryopoiesis and platelet formation. These genes show megakaryocyte-specific gene expression patterns and extensive network connectivity. Using gene silencing in Danio rerio and Drosophila melanogaster, we identified 11 of the genes as novel regulators of blood cell formation. Taken together, our findings advance understanding of novel gene functions controlling fate-determining events during megakaryopoiesis and platelet formation, providing a new example of successful translation of GWAS to function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335296/" 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/PMC3335296/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gieger, Christian -- Radhakrishnan, Aparna -- Cvejic, Ana -- Tang, Weihong -- Porcu, Eleonora -- Pistis, Giorgio -- Serbanovic-Canic, Jovana -- Elling, Ulrich -- Goodall, Alison H -- Labrune, Yann -- Lopez, Lorna M -- Magi, Reedik -- Meacham, Stuart -- Okada, Yukinori -- Pirastu, Nicola -- Sorice, Rossella -- Teumer, Alexander -- Voss, Katrin -- Zhang, Weihua -- Ramirez-Solis, Ramiro -- Bis, Joshua C -- Ellinghaus, David -- Gogele, Martin -- Hottenga, Jouke-Jan -- Langenberg, Claudia -- Kovacs, Peter -- O'Reilly, Paul F -- Shin, So-Youn -- Esko, Tonu -- Hartiala, Jaana -- Kanoni, Stavroula -- Murgia, Federico -- Parsa, Afshin -- Stephens, Jonathan -- van der Harst, Pim -- Ellen van der Schoot, C -- Allayee, Hooman -- Attwood, Antony -- Balkau, Beverley -- Bastardot, Francois -- Basu, Saonli -- Baumeister, Sebastian E -- Biino, Ginevra -- Bomba, Lorenzo -- Bonnefond, Amelie -- Cambien, Francois -- Chambers, John C -- Cucca, Francesco -- D'Adamo, Pio -- Davies, Gail -- de Boer, Rudolf A -- de Geus, Eco J C -- Doring, Angela -- Elliott, Paul -- Erdmann, Jeanette -- Evans, David M -- Falchi, Mario -- Feng, Wei -- Folsom, Aaron R -- Frazer, Ian H -- Gibson, Quince D -- Glazer, Nicole L -- Hammond, Chris -- Hartikainen, Anna-Liisa -- Heckbert, Susan R -- Hengstenberg, Christian -- Hersch, Micha -- Illig, Thomas -- Loos, Ruth J F -- Jolley, Jennifer -- Khaw, Kay Tee -- Kuhnel, Brigitte -- Kyrtsonis, Marie-Christine -- Lagou, Vasiliki -- Lloyd-Jones, Heather -- Lumley, Thomas -- Mangino, Massimo -- Maschio, Andrea -- Mateo Leach, Irene -- McKnight, Barbara -- Memari, Yasin -- Mitchell, Braxton D -- Montgomery, Grant W -- Nakamura, Yusuke -- Nauck, Matthias -- Navis, Gerjan -- Nothlings, Ute -- Nolte, Ilja M -- Porteous, David J -- Pouta, Anneli -- Pramstaller, Peter P -- Pullat, Janne -- Ring, Susan M -- Rotter, Jerome I -- Ruggiero, Daniela -- Ruokonen, Aimo -- Sala, Cinzia -- Samani, Nilesh J -- Sambrook, Jennifer -- Schlessinger, David -- Schreiber, Stefan -- Schunkert, Heribert -- Scott, James -- Smith, Nicholas L -- Snieder, Harold -- Starr, John M -- Stumvoll, Michael -- Takahashi, Atsushi -- Tang, W H Wilson -- Taylor, Kent -- Tenesa, Albert -- Lay Thein, Swee -- Tonjes, Anke -- Uda, Manuela -- Ulivi, Sheila -- van Veldhuisen, Dirk J -- Visscher, Peter M -- Volker, Uwe -- Wichmann, H-Erich -- Wiggins, Kerri L -- Willemsen, Gonneke -- Yang, Tsun-Po -- Hua Zhao, Jing -- Zitting, Paavo -- Bradley, John R -- Dedoussis, George V -- Gasparini, Paolo -- Hazen, Stanley L -- Metspalu, Andres -- Pirastu, Mario -- Shuldiner, Alan R -- Joost van Pelt, L -- Zwaginga, Jaap-Jan -- Boomsma, Dorret I -- Deary, Ian J -- Franke, Andre -- Froguel, Philippe -- Ganesh, Santhi K -- Jarvelin, Marjo-Riitta -- Martin, Nicholas G -- Meisinger, Christa -- Psaty, Bruce M -- Spector, Timothy D -- Wareham, Nicholas J -- Akkerman, Jan-Willem N -- Ciullo, Marina -- Deloukas, Panos -- Greinacher, Andreas -- Jupe, Steve -- Kamatani, Naoyuki -- Khadake, Jyoti -- Kooner, Jaspal S -- Penninger, Josef -- Prokopenko, Inga -- Stemple, Derek -- Toniolo, Daniela -- Wernisch, Lorenz -- Sanna, Serena -- Hicks, Andrew A -- Rendon, Augusto -- Ferreira, Manuel A -- Ouwehand, Willem H -- Soranzo, Nicole -- 092731/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BB/F019394/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- CZB/4/505/Chief Scientist Office/United Kingdom -- ETM/55/Chief Scientist Office/United Kingdom -- G0000111/Medical Research Council/United Kingdom -- G0601966/Medical Research Council/United Kingdom -- G0700704/Medical Research Council/United Kingdom -- G0700931/Medical Research Council/United Kingdom -- G0701120/Medical Research Council/United Kingdom -- G0701863/Medical Research Council/United Kingdom -- G0801056/Medical Research Council/United Kingdom -- G1000143/Medical Research Council/United Kingdom -- K12 RR023250/RR/NCRR NIH HHS/ -- K12 RR023250-05/RR/NCRR NIH HHS/ -- M01 RR016500/RR/NCRR NIH HHS/ -- M01 RR016500-08/RR/NCRR NIH HHS/ -- MC_U105260799/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106188470/Medical Research Council/United Kingdom -- N01 HC055015/HC/NHLBI NIH HHS/ -- N01 HC055016/HC/NHLBI NIH HHS/ -- N01 HC055018/HC/NHLBI NIH HHS/ -- N01 HC055019/HC/NHLBI NIH HHS/ -- N01 HC055020/HC/NHLBI NIH HHS/ -- N01 HC055021/HC/NHLBI NIH HHS/ -- N01 HC055022/HC/NHLBI NIH HHS/ -- N01 HC085079/HC/NHLBI NIH HHS/ -- P01 HL076491/HL/NHLBI NIH HHS/ -- P01 HL076491-09/HL/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- P01 HL098055-03/HL/NHLBI NIH HHS/ -- P30 DK072488/DK/NIDDK NIH HHS/ -- P30 DK072488-08/DK/NIDDK NIH HHS/ -- P41 HG003751/HG/NHGRI NIH HHS/ -- R01 AG018728/AG/NIA NIH HHS/ -- R01 AG018728-05S1/AG/NIA NIH HHS/ -- R01 GM053275/GM/NIGMS NIH HHS/ -- R01 GM053275-14/GM/NIGMS NIH HHS/ -- R01 HD042157/HD/NICHD NIH HHS/ -- R01 HD042157-01A1/HD/NICHD NIH HHS/ -- R01 HL059367/HL/NHLBI NIH HHS/ -- R01 HL059367-11/HL/NHLBI NIH HHS/ -- R01 HL068986/HL/NHLBI NIH HHS/ -- R01 HL068986-06/HL/NHLBI NIH HHS/ -- R01 HL073410/HL/NHLBI NIH HHS/ -- R01 HL073410-08/HL/NHLBI NIH HHS/ -- R01 HL085251/HL/NHLBI NIH HHS/ -- R01 HL085251-04/HL/NHLBI NIH HHS/ -- R01 HL086694/HL/NHLBI NIH HHS/ -- R01 HL086694-05/HL/NHLBI NIH HHS/ -- R01 HL087641/HL/NHLBI NIH HHS/ -- R01 HL087641-03/HL/NHLBI NIH HHS/ -- R01 HL087679-03/HL/NHLBI NIH HHS/ -- R01 HL088119/HL/NHLBI NIH HHS/ -- R01 HL088119-04/HL/NHLBI NIH HHS/ -- R01 HL103866/HL/NHLBI NIH HHS/ -- R01 HL103866-03/HL/NHLBI NIH HHS/ -- R01 HL105756/HL/NHLBI NIH HHS/ -- RG/09/012/28096/British Heart Foundation/United Kingdom -- RL1 MH083268/MH/NIMH NIH HHS/ -- RL1 MH083268-05/MH/NIMH NIH HHS/ -- U01 GM074518/GM/NIGMS NIH HHS/ -- U01 GM074518-04/GM/NIGMS NIH HHS/ -- U01 HL072515/HL/NHLBI NIH HHS/ -- U01 HL072515-06/HL/NHLBI NIH HHS/ -- U01 HL084756/HL/NHLBI NIH HHS/ -- U01 HL084756-03/HL/NHLBI NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- U54 RR020278-06/RR/NCRR NIH HHS/ -- UL1 RR025005/RR/NCRR NIH HHS/ -- UL1 RR025005-05/RR/NCRR NIH HHS/ -- WT077037/Z/05/Z/Wellcome Trust/United Kingdom -- WT077047/Z/05/Z/Wellcome Trust/United Kingdom -- WT082597/Z/07/Z/Wellcome Trust/United Kingdom -- England -- Nature. 2011 Nov 30;480(7376):201-8. doi: 10.1038/nature10659.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Genetic Epidemiology, Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Ingolstadter Landstr 1, 85764 Neuherberg, Germany. christian.gieger@helmholtz-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22139419" target="_blank"〉PubMed〈/a〉

Description: The formation of planets around binary stars may be more difficult than around single stars. In a close binary star (with a separation of less than a hundred astronomical units), theory predicts the presence of circumstellar disks around each star, and an outer circumbinary disk surrounding a gravitationally cleared inner cavity around the stars. Given that the inner disks are depleted by accretion onto the stars on timescales of a few thousand years, any replenishing material must be transferred from the outer reservoir to fuel planet formation (which occurs on timescales of about one million years). Gas flowing through disk cavities has been detected in single star systems. A circumbinary disk was discovered around the young low-mass binary system GG Tau A (ref. 7), which has recently been shown to be a hierarchical triple system. It has one large inner disk around the single star, GG Tau Aa, and shows small amounts of shocked hydrogen gas residing within the central cavity, but other than a single weak detection, the distribution of cold gas in this cavity or in any other binary or multiple star system has not hitherto been determined. Here we report imaging of gas fragments emitting radiation characteristic of carbon monoxide within the GG Tau A cavity. From the kinematics we conclude that the flow appears capable of sustaining the inner disk (around GG Tau Aa) beyond the accretion lifetime, leaving time for planet formation to occur there. These results show the complexity of planet formation around multiple stars and confirm the general picture predicted by numerical simulations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dutrey, Anne -- Di Folco, Emmanuel -- Guilloteau, Stephane -- Boehler, Yann -- Bary, Jeff -- Beck, Tracy -- Beust, Herve -- Chapillon, Edwige -- Gueth, Frederic -- Hure, Jean-Marc -- Pierens, Arnaud -- Pietu, Vincent -- Simon, Michal -- Tang, Ya-Wen -- England -- Nature. 2014 Oct 30;514(7524):600-2. doi: 10.1038/nature13822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Universite de Bordeaux, LAB, UMR 5804, F-33270 Floirac, France [2] Centre National de la Recherche Scientifique (CNRS), LAB, UMR 5804, F-33270 Floirac, France. ; Centro de Radioastronomia y Astrofisica (CRyA), University of Mexico, Apartado Postal 3-72, 58089 Morelia, Michoacan, Mexico. ; Department of Physics and Astronomy, Colgate University, 13 Oak Drive, Hamilton, New York 13346, USA. ; Space Telescope Science Institute, 3700 San Martin Drive, Baltimore, Maryland 21218, USA. ; Institut de Planetologie et d'Astrophysique de Grenoble (IPAG), UMR 5274, BP 53, F-38041 Grenoble Cedex 9, France. ; 1] Universite de Bordeaux, LAB, UMR 5804, F-33270 Floirac, France [2] Institut de RadioAstronomie Millimetrique (IRAM), 300 rue de la Piscine, F-38046 Saint Martin d'Heres, France. ; Institut de RadioAstronomie Millimetrique (IRAM), 300 rue de la Piscine, F-38046 Saint Martin d'Heres, France. ; Stony Brook University, Stony Brook, New York 11794-3800, USA. ; Academia Sinica Institute of Astronomy and Astrophysics, PO Box 23-141, Taipei 106, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25355359" target="_blank"〉PubMed〈/a〉

Description: Mammalian genomes contain several billion base pairs of DNA that are packaged in chromatin fibres. At selected gene loci, cohesin complexes have been proposed to arrange these fibres into higher-order structures, but how important this function is for determining overall chromosome architecture and how the process is regulated are not well understood. Using conditional mutagenesis in the mouse, here we show that depletion of the cohesin-associated protein Wapl stably locks cohesin on DNA, leads to clustering of cohesin in axial structures, and causes chromatin condensation in interphase chromosomes. These findings reveal that the stability of cohesin-DNA interactions is an important determinant of chromatin structure, and indicate that cohesin has an architectural role in interphase chromosome territories. Furthermore, we show that regulation of cohesin-DNA interactions by Wapl is important for embryonic development, expression of genes such as c-myc (also known as Myc), and cell cycle progression. In mitosis, Wapl-mediated release of cohesin from DNA is essential for proper chromosome segregation and protects cohesin from cleavage by the protease separase, thus enabling mitotic exit in the presence of functional cohesin complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tedeschi, Antonio -- Wutz, Gordana -- Huet, Sebastien -- Jaritz, Markus -- Wuensche, Annelie -- Schirghuber, Erika -- Davidson, Iain Finley -- Tang, Wen -- Cisneros, David A -- Bhaskara, Venugopal -- Nishiyama, Tomoko -- Vaziri, Alipasha -- Wutz, Anton -- Ellenberg, Jan -- Peters, Jan-Michael -- England -- Nature. 2013 Sep 26;501(7468):564-8. doi: 10.1038/nature12471. Epub 2013 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23975099" target="_blank"〉PubMed〈/a〉

Description: Nanog, a core pluripotency factor in the inner cell mass of blastocysts, is also expressed in unipotent primordial germ cells (PGCs) in mice, where its precise role is yet unclear. We investigated this in an in vitro model, in which naive pluripotent embryonic stem (ES) cells cultured in basic fibroblast growth factor (bFGF) and activin A develop as epiblast-like cells (EpiLCs) and gain competence for a PGC-like fate. Consequently, bone morphogenetic protein 4 (BMP4), or ectopic expression of key germline transcription factors Prdm1, Prdm14 and Tfap2c, directly induce PGC-like cells (PGCLCs) in EpiLCs, but not in ES cells. Here we report an unexpected discovery that Nanog alone can induce PGCLCs in EpiLCs, independently of BMP4. We propose that after the dissolution of the naive ES-cell pluripotency network during establishment of EpiLCs, the epigenome is reset for cell fate determination. Indeed, we found genome-wide changes in NANOG-binding patterns between ES cells and EpiLCs, indicating epigenetic resetting of regulatory elements. Accordingly, we show that NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by Prdm1) then directly induces Tfap2c. Furthermore, while SOX2 and NANOG promote the pluripotent state in ES cells, they show contrasting roles in EpiLCs, as Sox2 specifically represses PGCLC induction by Nanog. This study demonstrates a broadly applicable mechanistic principle for how cells acquire competence for cell fate determination, resulting in the context-dependent roles of key transcription factors during development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724940/" 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/PMC4724940/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murakami, Kazuhiro -- Gunesdogan, Ufuk -- Zylicz, Jan J -- Tang, Walfred W C -- Sengupta, Roopsha -- Kobayashi, Toshihiro -- Kim, Shinseog -- Butler, Richard -- Dietmann, Sabine -- Surani, M Azim -- 092096/Wellcome Trust/United Kingdom -- C6946/A14492/Cancer Research UK/United Kingdom -- RG44593/Wellcome Trust/United Kingdom -- WT096738/Wellcome Trust/United Kingdom -- England -- Nature. 2016 Jan 21;529(7586):403-7. doi: 10.1038/nature16480. Epub 2016 Jan 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK. ; Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK. ; Wellcome Trust Medical Research Council Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK. ; Laboratory for Pluripotent Cell Studies, Center for Developmental Biology, RIKEN, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan. ; Laboratory for Molecular and Cellular Biology, Faculty of Advanced Life Science, Hokkaido University, Kita21 Nishi11, Kita-ku, Sapporo, Hokkaido 001-0021, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26751055" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wenzhe -- England -- Nature. 2016 Apr 7;532(7597):37. doi: 10.1038/532037d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tsinghua University, Beijing, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078557" target="_blank"〉PubMed〈/a〉