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  • 1
    Publication Date: 1990-11-09
    Description: Anterior-specific neural induction can be assayed by means of an antibody that recognizes the Xenopus homeobox-containing protein En-2. The En-2 antigen is an excellent early marker, since it is present as a discrete band in the anterior neural plate of neurula embryos. Regional induction was assayed by combining dorsal mesoderm with competent ectoderm. Anterior notochord from the early neurula induced En-2 frequently, while posterior notochord induced En-2 less frequently. Presumptive somitic mesoderm and presumptive head mesoderm, though they induced neural tissue, were not strong inducers of En-2. Thus, anterior notochord may be the primary mesodermal tissue responsible for the patterning of the anterior neural plate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemmati-Brivanlou, A -- Stewart, R M -- Harland, R M -- GM 19363/GM/NIGMS NIH HHS/ -- GM 42341/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):800-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1978411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation ; *Genes, Homeobox ; Notochord/*physiology ; Transcription Factors/*blood/genetics ; Xenopus/*embryology/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-02-02
    Description: Receptor-interacting protein kinase 4 (RIPK4) is required for epidermal differentiation and is mutated in Bartsocas-Papas syndrome. RIPK4 binds to protein kinase C, but its signaling mechanisms are largely unknown. Ectopic RIPK4, but not catalytically inactive or Bartsocas-Papas RIPK4 mutants, induced accumulation of cytosolic beta-catenin and a transcriptional program similar to that caused by Wnt3a. In Xenopus embryos, Ripk4 synergized with coexpressed Xwnt8, whereas Ripk4 morpholinos or catalytic inactive Ripk4 antagonized Wnt signaling. RIPK4 interacted constitutively with the adaptor protein DVL2 and, after Wnt3a stimulation, with the co-receptor LRP6. Phosphorylation of DVL2 by RIPK4 favored canonical Wnt signaling. Wnt-dependent growth of xenografted human tumor cells was suppressed by RIPK4 knockdown, suggesting that RIPK4 overexpression may contribute to the growth of certain tumor types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094295/" 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/PMC4094295/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, XiaoDong -- McGann, James C -- Liu, Bob Y -- Hannoush, Rami N -- Lill, Jennie R -- Pham, Victoria -- Newton, Kim -- Kakunda, Michael -- Liu, Jinfeng -- Yu, Christine -- Hymowitz, Sarah G -- Hongo, Jo-Anne -- Wynshaw-Boris, Anthony -- Polakis, Paul -- Harland, Richard M -- Dixit, Vishva M -- R01 GM042341/GM/NIGMS NIH HHS/ -- R01 NS073159/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1441-5. doi: 10.1126/science.1232253. Epub 2013 Jan 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23371553" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*metabolism ; Animals ; Cell Line ; Cell Line, Tumor ; Cytosol/metabolism ; Female ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Low Density Lipoprotein Receptor-Related Protein-6/metabolism ; Neoplasm Transplantation ; Neoplasms/metabolism ; Ovarian Neoplasms/metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Transplantation, Heterologous ; *Wnt Signaling Pathway ; Wnt3A Protein/metabolism ; Xenopus Proteins/genetics/*metabolism ; Xenopus laevis/embryology/metabolism ; beta Catenin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1998-06-20
    Description: Noggin is a bone morphogenetic protein (BMP) antagonist expressed in Spemann's organizer. Murine Noggin is expressed in condensing cartilage and immature chondrocytes, as are many BMPs. In mice lacking Noggin, cartilage condensations initiated normally but developed hyperplasia, and initiation of joint development failed as measured by the expression of growth and differentiation factor-5. The maturation of cartilage and Hoxd expression were unaffected. Excess BMP activity in the absence of Noggin antagonism may enhance the recruitment of cells into cartilage, resulting in oversized growth plates; chondrocytes are also refractory to joint-inducing positional cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, L J -- McMahon, J A -- McMahon, A P -- Harland, R M -- GM49346/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 May 29;280(5368):1455-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9603738" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/genetics/metabolism ; Carrier Proteins ; Cartilage/*embryology/*metabolism ; Chondrocytes/metabolism ; Embryo, Mammalian/metabolism ; Extremities/*embryology ; Gene Expression ; Growth Differentiation Factor 5 ; Growth Substances/genetics ; Homeodomain Proteins/genetics ; Joints/abnormalities/*embryology ; Mesoderm/metabolism ; Mice ; Mice, Knockout ; Morphogenesis ; Mutation ; Proteins/*genetics/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2011-11-15
    Description: So far, two genes associated with familial melanoma have been identified, accounting for a minority of genetic risk in families. Mutations in CDKN2A account for approximately 40% of familial cases, and predisposing mutations in CDK4 have been reported in a very small number of melanoma kindreds. Here we report the whole-genome sequencing of probands from several melanoma families, which we performed in order to identify other genes associated with familial melanoma. We identify one individual carrying a novel germline variant (coding DNA sequence c.G1075A; protein sequence p.E318K; rs149617956) in the melanoma-lineage-specific oncogene microphthalmia-associated transcription factor (MITF). Although the variant co-segregated with melanoma in some but not all cases in the family, linkage analysis of 31 families subsequently identified to carry the variant generated a log of odds (lod) score of 2.7 under a dominant model, indicating E318K as a possible intermediate risk variant. Consistent with this, the E318K variant was significantly associated with melanoma in a large Australian case-control sample. Likewise, it was similarly associated in an independent case-control sample from the United Kingdom. In the Australian sample, the variant allele was significantly over-represented in cases with a family history of melanoma, multiple primary melanomas, or both. The variant allele was also associated with increased naevus count and non-blue eye colour. Functional analysis of E318K showed that MITF encoded by the variant allele had impaired sumoylation and differentially regulated several MITF targets. These data indicate that MITF is a melanoma-predisposition gene and highlight the utility of whole-genome sequencing to identify novel rare variants associated with disease susceptibility.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266855/" 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/PMC3266855/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, Satoru -- Woods, Susan L -- Boyle, Glen M -- Aoude, Lauren G -- MacGregor, Stuart -- Zismann, Victoria -- Gartside, Michael -- Cust, Anne E -- Haq, Rizwan -- Harland, Mark -- Taylor, John C -- Duffy, David L -- Holohan, Kelly -- Dutton-Regester, Ken -- Palmer, Jane M -- Bonazzi, Vanessa -- Stark, Mitchell S -- Symmons, Judith -- Law, Matthew H -- Schmidt, Christopher -- Lanagan, Cathy -- O'Connor, Linda -- Holland, Elizabeth A -- Schmid, Helen -- Maskiell, Judith A -- Jetann, Jodie -- Ferguson, Megan -- Jenkins, Mark A -- Kefford, Richard F -- Giles, Graham G -- Armstrong, Bruce K -- Aitken, Joanne F -- Hopper, John L -- Whiteman, David C -- Pharoah, Paul D -- Easton, Douglas F -- Dunning, Alison M -- Newton-Bishop, Julia A -- Montgomery, Grant W -- Martin, Nicholas G -- Mann, Graham J -- Bishop, D Timothy -- Tsao, Hensin -- Trent, Jeffrey M -- Fisher, David E -- Hayward, Nicholas K -- Brown, Kevin M -- 10118/Cancer Research UK/United Kingdom -- 10589/Cancer Research UK/United Kingdom -- AR043369-14/AR/NIAMS NIH HHS/ -- C490/A11021/Cancer Research UK/United Kingdom -- C588/A10589/Cancer Research UK/United Kingdom -- C588/A4994/Cancer Research UK/United Kingdom -- C8197/A10123/Cancer Research UK/United Kingdom -- C8216/A6129/Cancer Research UK/United Kingdom -- CA88363/CA/NCI NIH HHS/ -- K24CA149202/CA/NCI NIH HHS/ -- P50CA9368/CA/NCI NIH HHS/ -- R01 AR043369/AR/NIAMS NIH HHS/ -- R01 CA-83115-01A2/CA/NCI NIH HHS/ -- R01 CA088363/CA/NCI NIH HHS/ -- R01 CA088363-09/CA/NCI NIH HHS/ -- R01 CA83115/CA/NCI NIH HHS/ -- England -- Nature. 2011 Nov 13;480(7375):99-103. doi: 10.1038/nature10630.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22080950" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Female ; Gene Expression Regulation, Neoplastic ; *Genetic Predisposition to Disease ; Humans ; Male ; Melanoma/*genetics ; Microphthalmia-Associated Transcription Factor/*genetics ; Middle Aged ; *Mutation ; Sumoylation/genetics ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-07-21
    Description: Author(s): E. A. Stepanov, S. Brener, F. Krien, M. Harland, A. I. Lichtenstein, and M. I. Katsnelson We consider the extended Hubbard model and introduce a corresponding Heisenberg-like problem written in terms of spin operators. The derived formalism is reminiscent of Anderson’s idea of the effective exchange interaction and takes into account nonlocal correlation effects. The results for the exch... [Phys. Rev. Lett. 121, 037204] Published Fri Jul 20, 2018
    Keywords: Condensed Matter: Electronic Properties, etc.
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
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  • 6
    Publication Date: 1993-10-29
    Description: The Spermann organizer induces neural tissue from dorsal ectoderm and dorsalizes lateral and ventral mesoderm in Xenopus. The secreted factor noggin, which is expressed in the organizer, can mimic the dorsalizing signal of the organizer. Data are presented showing that noggin directly induces neural tissue, that it induces neural tissue in the absence of dorsal mesoderm, and that it acts at the appropriate stage to be an endogenous neural inducing signal. Noggin induces cement glands and anterior brain markers, but not hindbrain or spinal cord markers. Thus, noggin has the expression pattern and activity expected of an endogenous neural inducer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamb, T M -- Knecht, A K -- Smith, W C -- Stachel, S E -- Economides, A N -- Stahl, N -- Yancopolous, G D -- Harland, R M -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):713-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; CHO Cells ; Carrier Proteins ; Cricetinae ; Embryonic Induction/*physiology ; Gastrula/metabolism ; Humans ; Mesoderm/metabolism ; Nervous System/*embryology ; Proteins/*physiology ; RNA, Messenger/metabolism ; Recombinant Proteins ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2010-05-01
    Description: The western clawed frog Xenopus tropicalis is an important model for vertebrate development that combines experimental advantages of the African clawed frog Xenopus laevis with more tractable genetics. Here we present a draft genome sequence assembly of X. tropicalis. This genome encodes more than 20,000 protein-coding genes, including orthologs of at least 1700 human disease genes. Over 1 million expressed sequence tags validated the annotation. More than one-third of the genome consists of transposable elements, with unusually prevalent DNA transposons. Like that of other tetrapods, the genome of X. tropicalis contains gene deserts enriched for conserved noncoding elements. The genome exhibits substantial shared synteny with human and chicken over major parts of large chromosomes, broken by lineage-specific chromosome fusions and fissions, mainly in the mammalian lineage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994648/" 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/PMC2994648/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hellsten, Uffe -- Harland, Richard M -- Gilchrist, Michael J -- Hendrix, David -- Jurka, Jerzy -- Kapitonov, Vladimir -- Ovcharenko, Ivan -- Putnam, Nicholas H -- Shu, Shengqiang -- Taher, Leila -- Blitz, Ira L -- Blumberg, Bruce -- Dichmann, Darwin S -- Dubchak, Inna -- Amaya, Enrique -- Detter, John C -- Fletcher, Russell -- Gerhard, Daniela S -- Goodstein, David -- Graves, Tina -- Grigoriev, Igor V -- Grimwood, Jane -- Kawashima, Takeshi -- Lindquist, Erika -- Lucas, Susan M -- Mead, Paul E -- Mitros, Therese -- Ogino, Hajime -- Ohta, Yuko -- Poliakov, Alexander V -- Pollet, Nicolas -- Robert, Jacques -- Salamov, Asaf -- Sater, Amy K -- Schmutz, Jeremy -- Terry, Astrid -- Vize, Peter D -- Warren, Wesley C -- Wells, Dan -- Wills, Andrea -- Wilson, Richard K -- Zimmerman, Lyle B -- Zorn, Aaron M -- Grainger, Robert -- Grammer, Timothy -- Khokha, Mustafa K -- Richardson, Paul M -- Rokhsar, Daniel S -- HHSN261200800001E/CA/NCI NIH HHS/ -- MC_U117560482/Medical Research Council/United Kingdom -- P41 HD064556/HD/NICHD NIH HHS/ -- P41 HD064556-01/HD/NICHD NIH HHS/ -- P41 HD064556-02/HD/NICHD NIH HHS/ -- R01 AI027877/AI/NIAID NIH HHS/ -- R01 AI027877-20/AI/NIAID NIH HHS/ -- R01 DK070858/DK/NIDDK NIH HHS/ -- R01 DK070858-05/DK/NIDDK NIH HHS/ -- R01 EY018000/EY/NEI NIH HHS/ -- R01 EY018000-03/EY/NEI NIH HHS/ -- R01 GM060572/GM/NIGMS NIH HHS/ -- R01 GM060572-05/GM/NIGMS NIH HHS/ -- R01 GM086321/GM/NIGMS NIH HHS/ -- R01 GM086321-03/GM/NIGMS NIH HHS/ -- R01 HD042294/HD/NICHD NIH HHS/ -- R01 HD042294-05/HD/NICHD NIH HHS/ -- R01 HD045776/HD/NICHD NIH HHS/ -- R01 HD045776-05/HD/NICHD NIH HHS/ -- R01 HD046661-03/HD/NICHD NIH HHS/ -- R01 MH079381/MH/NIMH NIH HHS/ -- R01 MH079381-02/MH/NIMH NIH HHS/ -- R21 HD065713/HD/NICHD NIH HHS/ -- R24 AI059830/AI/NIAID NIH HHS/ -- R24 AI059830-08/AI/NIAID NIH HHS/ -- R24 RR015088/RR/NCRR NIH HHS/ -- R24 RR015088-03/RR/NCRR NIH HHS/ -- U01 HG002155-05/HG/NHGRI NIH HHS/ -- U01 HG02155/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 30;328(5978):633-6. doi: 10.1126/science.1183670.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA. uhellsten@lbl.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20431018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens/genetics ; Chromosome Mapping ; Chromosomes/genetics ; Computational Biology ; Conserved Sequence ; DNA Transposable Elements ; DNA, Complementary ; Embryo, Nonmammalian/metabolism ; Evolution, Molecular ; Expressed Sequence Tags ; Gene Duplication ; Genes ; *Genome ; Humans ; Phylogeny ; *Sequence Analysis, DNA ; Synteny ; Vertebrates/genetics ; Xenopus/embryology/*genetics ; Xenopus Proteins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2016-10-20
    Description: Genome evolution in the allotetraploid frog Xenopus laevis Nature 538, 7625 (2016). doi:10.1038/nature19840 Authors: Adam M. Session, Yoshinobu Uno, Taejoon Kwon, Jarrod A. Chapman, Atsushi Toyoda, Shuji Takahashi, Akimasa Fukui, Akira Hikosaka, Atsushi Suzuki, Mariko Kondo, Simon J. van Heeringen, Ian Quigley, Sven Heinz, Hajime Ogino, Haruki Ochi, Uffe Hellsten, Jessica B. Lyons, Oleg Simakov, Nicholas Putnam, Jonathan Stites, Yoko Kuroki, Toshiaki Tanaka, Tatsuo Michiue, Minoru Watanabe, Ozren Bogdanovic, Ryan Lister, Georgios Georgiou, Sarita S. Paranjpe, Ila van Kruijsbergen, Shengquiang Shu, Joseph Carlson, Tsutomu Kinoshita, Yuko Ohta, Shuuji Mawaribuchi, Jerry Jenkins, Jane Grimwood, Jeremy Schmutz, Therese Mitros, Sahar V. Mozaffari, Yutaka Suzuki, Yoshikazu Haramoto, Takamasa S. Yamamoto, Chiyo Takagi, Rebecca Heald, Kelly Miller, Christian Haudenschild, Jacob Kitzman, Takuya Nakayama, Yumi Izutsu, Jacques Robert, Joshua Fortriede, Kevin Burns, Vaneet Lotay, Kamran Karimi, Yuuri Yasuoka, Darwin S. Dichmann, Martin F. Flajnik, Douglas W. Houston, Jay Shendure, Louis DuPasquier, Peter D. Vize, Aaron M. Zorn, Michihiko Ito, Edward M. Marcotte, John B. Wallingford, Yuzuru Ito, Makoto Asashima, Naoto Ueno, Yoichi Matsuda, Gert Jan C. Veenstra, Asao Fujiyama, Richard M. Harland, Masanori Taira & Daniel S. Rokhsar To explore the origins and consequences of tetraploidy in the African clawed frog, we sequenced the Xenopus laevis genome and compared it to the related diploid X. tropicalis genome. We characterize the allotetraploid origin of X. laevis by partitioning its genome into
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 9
    Publication Date: 2017-01-04
    Description: To define a complete catalog of the genes that are activated during mouse sclerotome formation, we sequenced RNA from embryonic mouse tissue directed to form sclerotome in culture. In addition to well-known early markers of sclerotome, such as Pax1, Pax9, and the Bapx2/Nkx3-2 homolog Nkx3-1, the long-noncoding RNA PEAT (Pax1...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    ISSN: 1365-2486
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
    Notes: Polar forests once extended across the high-latitude landmasses during ice-free ‘greenhouse’ intervals in Earth history. In the Cretaceous ‘greenhouse’ world, Arctic conifer forests were considered predominantly deciduous, while those on Antarctica contained a significantly greater proportion of evergreens. To investigate the causes of this distinctive biogeographical pattern, we developed a coupled model of conifer growth, soil biogeochemistry and forest dynamics. Our approach emphasized general relationships between leaf lifespan (LL) and function, and incorporated the feedback of LL on soil nutrient status. The model was forced with a mid-Cretaceous ‘greenhouse’ climate simulated by the Hadley Centre GCM. Simulated polar forests contained mixtures of dominant LLs, which reproduced observed biogeographical patterns of deciduous, mixed and evergreen biomes. It emerged that disturbance by fire was a critical factor. Frequent fires in simulated Arctic ecosystems promoted the dominance of trees with short LLs that were characterized by the rapid growth and colonization rates typical of today's boreal pioneer species. In Antarctica, however, infrequent fires allowed trees with longer LLs to dominate because they attained greater height, despite slower growth rates. A direct test of the approach was successfully achieved by comparing modelled LLs with quantitative estimates using Cretaceous fossil woods from Svalbard in the European Arctic and Alexander Island, Antarctica. Observations and the model both revealed mixed Arctic and evergreen Antarctic communities with peak dominance of trees with the same LLs. Our study represents a significant departure from the long-held belief that leaf habit was an adaptation to warm, dark winter climates, and highlights a previously unrecognized role for disturbance (in whatever guise) in polar forest ecology.
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