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  • 1
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    The Small Nuclear Genomes of Selaginella Are Associated with a Low Rate of Genome Size Evolution (2016)
    Oxford University Press
    Details
    Publication Date: 2016-06-05
    Description: The haploid nuclear genome size (1C DNA) of vascular land plants varies over several orders of magnitude. Much of this observed diversity in genome size is due to the proliferation and deletion of transposable elements. To date, all vascular land plant lineages with extremely small nuclear genomes represent recently derived states, having ancestors with much larger genome sizes. The Selaginellaceae represent an ancient lineage with extremely small genomes. It is unclear how small nuclear genomes evolved in Selaginella . We compared the rates of nuclear genome size evolution in Selaginella and major vascular plant clades in a comparative phylogenetic framework. For the analyses, we collected 29 new flow cytometry estimates of haploid genome size in Selaginella to augment publicly available data. Selaginella possess some of the smallest known haploid nuclear genome sizes, as well as the lowest rate of genome size evolution observed across all vascular land plants included in our analyses. Additionally, our analyses provide strong support for a history of haploid nuclear genome size stasis in Selaginella . Our results indicate that Selaginella , similar to other early diverging lineages of vascular land plants, has relatively low rates of genome size evolution. Further, our analyses highlight that a rapid transition to a small genome size is only one route to an extremely small genome.
    Electronic ISSN: 1759-6653
    Topics: Biology
    Published by Oxford University Press
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  • 2
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    The last 2 Myr of accretionary wedge construction in the central Hikurangi margin (North Island, New Zealand): Insights from structural modeling (2016)
    Wiley
    Details
    Publication Date: 2016-06-19
    Description: Three depth-converted and geologically interpreted seismic profiles provide a clear image of the offshore outer accretionary wedge associated with oblique subduction of the Pacific Plate beneath the central Hikurangi margin. Plio-Quaternary turbidites deposited over the pelagic cover sequence of the Hikurangi Plateau have been accreted to the margin by imbrication along E-verging thrust faults that propagated up-section from the plate boundary décollement. Growth stratigraphy of piggy-back basins and thrusting of progressively younger horizons trace the eastward advance of the leading thrust front over c. 60 km in the last 2 Myr. Moderate internal shortening of fault-bounded blocks typically 4-8 km wide reflects rapid creation of thrust faults, with some early formed faults undergoing out-of-sequence reactivation to maintain critical wedge taper. Multi-stage structural restorations show that forward progression of shortening involves: (1) initial development of a c. 10-25 km wide “proto-thrust” zone, comprising conjugate sets of moderately to steeply dipping low-displacement (c. 10-100 m) reverse faults; and (2) growth of thrust faults that exploit some of the early proto-thrust faults and propagate up-section with progressive break-through of folds localized above the fault tips. The youngest, still unbreached folds deform the present-day seafloor. Progressive retro-deformations show that macroscopic thrust faults and folds account for less than 50% of the margin-perpendicular shortening imposed by plate convergence. Arguably, significant fractions of the missing components can be attributed to meso- and microscopic scale layer-parallel shortening within the wedge, in the proto-thrust zones, and in the outer décollement zone. This article is protected by copyright. All rights reserved.
    Electronic ISSN: 1525-2027
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 3
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    Oligocene-Miocene spreading history of the northern South Fiji Basin and implications for the evolution of the New Zealand plate boundary (2011)
    Wiley
    Details
    Publication Date: 2011-02-09
    Description: A tectonic model of the evolution of the northern half of the South Fiji Basin, including the Minerva Triple Junction and Cook Fracture Zone, is developed from regional gravity, multibeam bathymetry, and a new interpretation of magnetic anomalies pinned to radiometric dates of oceanic crust in the basin. The geometry and age of a portion of the Minerva Triple Junction and the Cook-Minerva spreading center (the connection from the triple junction to the Cook Fracture Zone, which accommodated coeval opening of the Norfolk Basin), are resolved with multibeam bathymetry and magnetics. The South Fiji Basin opened from about 34 to 15 Ma in an anticlockwise sweep about an Euler pole located at the northern end of the present Lau Ridge. This rotation and a rigidly straight southeastward motion of the Three Kings Ridge were accommodated by the configuration of the triple junction changing from ridge-fault-fault to ridge-ridge-fault to ridge-ridge-ridge. During this evolution the southeastern arm of the system, the Julia Fracture Zone, underwent several transformations and the Cook-Minerva spreading center experienced repeated ridge jumps. The kinematics of the northern South Fiji Basin dictate, to a large extent, the evolution of the southern South Fiji Basin and the Norfolk Basin. This in turn leads to the interpretation of a complex trench-trench-double transform fault framework at the northern New Zealand margin, which explains most aspects of the geology, structure, and arc volcanic history of the margin and provides a radical new setting for the origin of the Northland Allochthon.
    Electronic ISSN: 1525-2027
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 4
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    Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Genome-wide meta-analysis implicates mediators of hair follicle development and morphogenesis in risk for severe acne (2018)
    Christos Petridis; Alexander A. Navarini; Nick Dand; Jake Saklatvala; David Baudry; Michael Duckworth; Michael H. Allen; Charles J. Curtis; Sang Hyuck Lee; A. David Burden; Alison Layton; Veronique Bataille; Andrew E. Pink; Anton Alexandroff; Alex Anstey; Jaskiran Azad; Omar Aziz; Nigel Burrows; Aamir Butt; Peter Cartwright; Anna Chapman; Timothy H. Clayton; Sandeep Cliff; Tim Cutler; Brigid Daly; Amrit Darvay; Claudia De; Giovanni; Anthony Downs; Colm Dwyer; John English; Adam Ferguson; Colin Fleming; Elizabeth Fraser-Andrews; Mark Goodfield; Clive E. Grattan; Hartmut Hempel; Sue Hood; Bronwyn Hughes; Evmorfia Ladoyanni; Calum Lyon; Ali Mahmud; Moshin Malik; Eleanor Mallon; Simon Meggitt; Andrew Messenger; Yaaseen Moosa; Stephanie Munn; Anthony Ormerod; Deepak Rallan; Janet Ross; Ingrid Salvary; Rachel Wachsmuth; Shyamal Wahie; Shernaz Walton; Sarah Walsh; Diane Williamson; Carolyn Willis; Isabelle Carlavan; Johannes J. Voegel; Timothy D. Spector; Richard C. Trembath; John A. McGrath; Catherine H. Smith; Jonathan N. Barker; Michael A. Simpson
    Springer Nature
    Details
    Publication Date: 2018-12-13
    Description: Genome-wide meta-analysis implicates mediators of hair follicle development and morphogenesis in risk for severe acne Genome-wide meta-analysis implicates mediators of hair follicle development and morphogenesis in risk for severe acne, Published online: 12 December 2018; doi:10.1038/s41467-018-07459-5 Acne vulgaris is a chronic inflammation of the skin, the genetic basis of which is incompletely understood. Here, Petridis et al. perform GWAS and meta-analysis for acne in 26,722 individuals and identify 12 novel risk loci that implicate structure and maintenance of the skin in severe acne risk.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 6
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    Single Lgr5 stem cells build crypt-villus structures in vitro without a mesenchymal niche (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-03-31
    Description: The intestinal epithelium is the most rapidly self-renewing tissue in adult mammals. We have recently demonstrated the presence of about six cycling Lgr5(+) stem cells at the bottoms of small-intestinal crypts. Here we describe the establishment of long-term culture conditions under which single crypts undergo multiple crypt fission events, while simultanously generating villus-like epithelial domains in which all differentiated cell types are present. Single sorted Lgr5(+) stem cells can also initiate these cryptvillus organoids. Tracing experiments indicate that the Lgr5(+) stem-cell hierarchy is maintained in organoids. We conclude that intestinal cryptvillus units are self-organizing structures, which can be built from a single stem cell in the absence of a non-epithelial cellular niche.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Toshiro -- Vries, Robert G -- Snippert, Hugo J -- van de Wetering, Marc -- Barker, Nick -- Stange, Daniel E -- van Es, Johan H -- Abo, Arie -- Kujala, Pekka -- Peters, Peter J -- Clevers, Hans -- England -- Nature. 2009 May 14;459(7244):262-5. doi: 10.1038/nature07935. Epub 2009 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute and University Medical Center Utrecht, Uppsalalaan 8, 3584CT Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19329995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/*methods ; Cell Lineage ; Cell Separation ; Gene Expression Regulation, Developmental ; Intestines/*anatomy & histology/*cytology/metabolism ; Mesoderm/cytology/metabolism ; Mice ; Multipotent Stem Cells/cytology/metabolism ; Organoids/*cytology/growth & development/metabolism ; Paneth Cells/metabolism ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Regeneration ; Stem Cell Niche ; Stem Cells/*cytology/*metabolism
    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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  • 7
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    Crypt stem cells as the cells-of-origin of intestinal cancer (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-12-19
    Description: Intestinal cancer is initiated by Wnt-pathway-activating mutations in genes such as adenomatous polyposis coli (APC). As in most cancers, the cell of origin has remained elusive. In a previously established Lgr5 (leucine-rich-repeat containing G-protein-coupled receptor 5) knockin mouse model, a tamoxifen-inducible Cre recombinase is expressed in long-lived intestinal stem cells. Here we show that deletion of Apc in these stem cells leads to their transformation within days. Transformed stem cells remain located at crypt bottoms, while fuelling a growing microadenoma. These microadenomas show unimpeded growth and develop into macroscopic adenomas within 3-5weeks. The distribution of Lgr5(+) cells within stem-cell-derived adenomas indicates that a stem cell/progenitor cell hierarchy is maintained in early neoplastic lesions. When Apc is deleted in short-lived transit-amplifying cells using a different cre mouse, the growth of the induced microadenomas rapidly stalls. Even after 30weeks, large adenomas are very rare in these mice. We conclude that stem-cell-specific loss of Apc results in progressively growing neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, Nick -- Ridgway, Rachel A -- van Es, Johan H -- van de Wetering, Marc -- Begthel, Harry -- van den Born, Maaike -- Danenberg, Esther -- Clarke, Alan R -- Sansom, Owen J -- Clevers, Hans -- G0301154/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2009 Jan 29;457(7229):608-11. doi: 10.1038/nature07602. Epub 2008 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584CT Utrecht & University Medical Centre Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092804" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein/*deficiency/*genetics ; Animals ; *Cell Lineage ; Cell Proliferation ; *Cell Transformation, Neoplastic/genetics/pathology ; Colonic Neoplasms/genetics/metabolism/pathology ; Genes, APC ; Intestinal Neoplasms/*genetics/metabolism/*pathology ; Mice ; Neoplastic Stem Cells/metabolism/*pathology ; Receptors, G-Protein-Coupled/analysis/genetics/metabolism ; beta Catenin/metabolism
    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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  • 8
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    Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by beta-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of beta-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P J -- Sparks, A B -- Korinek, V -- Barker, N -- Clevers, H -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065402" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Germ-Line Mutation ; Humans ; Mutation ; Phosphorylation ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    Functional interaction between beta-catenin and FOXO in oxidative stress signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-21
    Description: beta-Catenin is a multifunctional protein that mediates Wnt signaling by binding to members of the T cell factor (TCF) family of transcription factors. Here, we report an evolutionarily conserved interaction of beta-catenin with FOXO transcription factors, which are regulated by insulin and oxidative stress signaling. beta-Catenin binds directly to FOXO and enhances FOXO transcriptional activity in mammalian cells. In Caenorhabditis elegans, loss of the beta-catenin BAR-1 reduces the activity of the FOXO ortholog DAF-16 in dauer formation and life span. Association of beta-catenin with FOXO was enhanced in cells exposed to oxidative stress. Furthermore, BAR-1 was required for the oxidative stress-induced expression of the DAF-16 target gene sod-3 and for resistance to oxidative damage. These results demonstrate a role for beta-catenin in regulating FOXO function that is particularly important under conditions of oxidative stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Essers, Marieke A G -- de Vries-Smits, Lydia M M -- Barker, Nick -- Polderman, Paulien E -- Burgering, Boudewijn M T -- Korswagen, Hendrik C -- New York, N.Y. -- Science. 2005 May 20;308(5725):1181-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry and Center for Biomedical Genetics, University Medical Center, Universiteitsweg 100, 3584 CG Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics/*metabolism/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/metabolism ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p27 ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Forkhead Transcription Factors ; Humans ; Hydrogen Peroxide/pharmacology ; Immunoprecipitation ; Insulin/pharmacology ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Lithium Chloride/pharmacology ; Longevity ; Mice ; Mutation ; *Oxidative Stress ; Receptor, Insulin/genetics/metabolism ; *Signal Transduction ; Superoxide Dismutase/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/*metabolism ; Transfection ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Paneth cells constitute the niche for Lgr5 stem cells in intestinal crypts (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-30
    Description: Homeostasis of self-renewing small intestinal crypts results from neutral competition between Lgr5 stem cells, which are small cycling cells located at crypt bottoms. Lgr5 stem cells are interspersed between terminally differentiated Paneth cells that are known to produce bactericidal products such as lysozyme and cryptdins/defensins. Single Lgr5-expressing stem cells can be cultured to form long-lived, self-organizing crypt-villus organoids in the absence of non-epithelial niche cells. Here we find a close physical association of Lgr5 stem cells with Paneth cells in mice, both in vivo and in vitro. CD24(+) Paneth cells express EGF, TGF-alpha, Wnt3 and the Notch ligand Dll4, all essential signals for stem-cell maintenance in culture. Co-culturing of sorted stem cells with Paneth cells markedly improves organoid formation. This Paneth cell requirement can be substituted by a pulse of exogenous Wnt. Genetic removal of Paneth cells in vivo results in the concomitant loss of Lgr5 stem cells. In colon crypts, CD24(+) cells residing between Lgr5 stem cells may represent the Paneth cell equivalents. We conclude that Lgr5 stem cells compete for essential niche signals provided by a specialized daughter cell, the Paneth cell.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547360/" 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/PMC3547360/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Toshiro -- van Es, Johan H -- Snippert, Hugo J -- Stange, Daniel E -- Vries, Robert G -- van den Born, Maaike -- Barker, Nick -- Shroyer, Noah F -- van de Wetering, Marc -- Clevers, Hans -- R01 CA142826/CA/NCI NIH HHS/ -- R01 CA142826-01/CA/NCI NIH HHS/ -- R03 DK084167/DK/NIDDK NIH HHS/ -- R03 DK084167-01/DK/NIDDK NIH HHS/ -- England -- Nature. 2011 Jan 20;469(7330):415-8. doi: 10.1038/nature09637. Epub 2010 Nov 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584CT Utrecht, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21113151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD24/metabolism ; Cell Count ; Cell Proliferation ; Coculture Techniques ; Humans ; Intestines/*cytology ; Mice ; Multipotent Stem Cells/*cytology/*metabolism ; Paneth Cells/*cytology/secretion ; Receptors, G-Protein-Coupled/*metabolism ; Stem Cell Niche/*cytology/secretion ; Wnt Proteins/metabolism/secretion ; Wnt3 Protein
    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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