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  • 1
    Publication Date: 2011-07-12
    Description: Potato (Solanum tuberosum L.) is the world's most important non-grain food crop and is central to global food security. It is clonally propagated, highly heterozygous, autotetraploid, and suffers acute inbreeding depression. Here we use a homozygous doubled-monoploid potato clone to sequence and assemble 86% of the 844-megabase genome. We predict 39,031 protein-coding genes and present evidence for at least two genome duplication events indicative of a palaeopolyploid origin. As the first genome sequence of an asterid, the potato genome reveals 2,642 genes specific to this large angiosperm clade. We also sequenced a heterozygous diploid clone and show that gene presence/absence variants and other potentially deleterious mutations occur frequently and are a likely cause of inbreeding depression. Gene family expansion, tissue-specific expression and recruitment of genes to new pathways contributed to the evolution of tuber development. The potato genome sequence provides a platform for genetic improvement of this vital crop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potato Genome Sequencing Consortium -- Xu, Xun -- Pan, Shengkai -- Cheng, Shifeng -- Zhang, Bo -- Mu, Desheng -- Ni, Peixiang -- Zhang, Gengyun -- Yang, Shuang -- Li, Ruiqiang -- Wang, Jun -- Orjeda, Gisella -- Guzman, Frank -- Torres, Michael -- Lozano, Roberto -- Ponce, Olga -- Martinez, Diana -- De la Cruz, German -- Chakrabarti, S K -- Patil, Virupaksh U -- Skryabin, Konstantin G -- Kuznetsov, Boris B -- Ravin, Nikolai V -- Kolganova, Tatjana V -- Beletsky, Alexey V -- Mardanov, Andrei V -- Di Genova, Alex -- Bolser, Daniel M -- Martin, David M A -- Li, Guangcun -- Yang, Yu -- Kuang, Hanhui -- Hu, Qun -- Xiong, Xingyao -- Bishop, Gerard J -- Sagredo, Boris -- Mejia, Nilo -- Zagorski, Wlodzimierz -- Gromadka, Robert -- Gawor, Jan -- Szczesny, Pawel -- Huang, Sanwen -- Zhang, Zhonghua -- Liang, Chunbo -- He, Jun -- Li, Ying -- He, Ying -- Xu, Jianfei -- Zhang, Youjun -- Xie, Binyan -- Du, Yongchen -- Qu, Dongyu -- Bonierbale, Merideth -- Ghislain, Marc -- Herrera, Maria del Rosario -- Giuliano, Giovanni -- Pietrella, Marco -- Perrotta, Gaetano -- Facella, Paolo -- O'Brien, Kimberly -- Feingold, Sergio E -- Barreiro, Leandro E -- Massa, Gabriela A -- Diambra, Luis -- Whitty, Brett R -- Vaillancourt, Brieanne -- Lin, Haining -- Massa, Alicia N -- Geoffroy, Michael -- Lundback, Steven -- DellaPenna, Dean -- Buell, C Robin -- Sharma, Sanjeev Kumar -- Marshall, David F -- Waugh, Robbie -- Bryan, Glenn J -- Destefanis, Marialaura -- Nagy, Istvan -- Milbourne, Dan -- Thomson, Susan J -- Fiers, Mark -- Jacobs, Jeanne M E -- Nielsen, Kare L -- Sonderkaer, Mads -- Iovene, Marina -- Torres, Giovana A -- Jiang, Jiming -- Veilleux, Richard E -- Bachem, Christian W B -- de Boer, Jan -- Borm, Theo -- Kloosterman, Bjorn -- van Eck, Herman -- Datema, Erwin -- Hekkert, Bas te Lintel -- Goverse, Aska -- van Ham, Roeland C H J -- Visser, Richard G F -- BB/F012640/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F012640/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT 083481/Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jul 10;475(7355):189-95. doi: 10.1038/nature10158.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BGI-Shenzhen, Chinese Ministry of Agricultural, Key Lab of Genomics, Beishan Industrial Zone, Yantian District, Shenzhen 518083, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21743474" target="_blank"〉PubMed〈/a〉
    Keywords: Evolution, Molecular ; Gene Duplication ; Gene Expression Regulation, Plant ; Genes, Plant/genetics ; Genetic Variation ; Genome, Plant/*genetics ; *Genomics ; Haplotypes/genetics ; Heterozygote ; Homozygote ; Immunity, Innate ; Inbreeding ; Molecular Sequence Annotation ; Molecular Sequence Data ; Plant Diseases/genetics ; Ploidies ; Solanum tuberosum/*genetics/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2016-03-25
    Description: Focal amplifications of chromosome 3p13-3p14 occur in about 10% of melanomas and are associated with a poor prognosis. The melanoma-specific oncogene MITF resides at the epicentre of this amplicon. However, whether other loci present in this amplicon also contribute to melanomagenesis is unknown. Here we show that the recently annotated long non-coding RNA (lncRNA) gene SAMMSON is consistently co-gained with MITF. In addition, SAMMSON is a target of the lineage-specific transcription factor SOX10 and its expression is detectable in more than 90% of human melanomas. Whereas exogenous SAMMSON increases the clonogenic potential in trans, SAMMSON knockdown drastically decreases the viability of melanoma cells irrespective of their transcriptional cell state and BRAF, NRAS or TP53 mutational status. Moreover, SAMMSON targeting sensitizes melanoma to MAPK-targeting therapeutics both in vitro and in patient-derived xenograft models. Mechanistically, SAMMSON interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function. Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted anti-melanoma therapeutic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leucci, Eleonora -- Vendramin, Roberto -- Spinazzi, Marco -- Laurette, Patrick -- Fiers, Mark -- Wouters, Jasper -- Radaelli, Enrico -- Eyckerman, Sven -- Leonelli, Carina -- Vanderheyden, Katrien -- Rogiers, Aljosja -- Hermans, Els -- Baatsen, Pieter -- Aerts, Stein -- Amant, Frederic -- Van Aelst, Stefan -- van den Oord, Joost -- de Strooper, Bart -- Davidson, Irwin -- Lafontaine, Denis L J -- Gevaert, Kris -- Vandesompele, Jo -- Mestdagh, Pieter -- Marine, Jean-Christophe -- England -- Nature. 2016 Mar 24;531(7595):518-22. doi: 10.1038/nature17161.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory For Molecular Cancer Biology, Center for Human Genetics, KULeuven, Herestraat 49, 3000 Leuven, Belgium. ; Center for the Biology of Disease, VIB, Herestraat 49, 3000 Leuven, Belgium. ; Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), Rue Laurent Fries 1, 67404 Illkirch, France. ; Laboratory of Translational Cell and Tissue Research, Department of Pathology, KULeuven and UZ Leuven, Herestraat 49, 3000 Leuven, Belgium. ; Mouse Histopathology Core Facility, Center for the Biology of Disease, VIB-KULeuven, Herestraat 49, 3000 Leuven, Belgium. ; Medical Biotechnology Center, VIB, Albert Baertsoenkaai 3, 9000 Gent, Belgium. ; Department of Biochemistry, Gent University, Albert Baertsoenkaai 3, 9000 Gent, Belgium. ; Center for Medical Genetics, Gent University, De Pintelaan 185, 9000 Gent, Belgium. ; Cancer Research Institute Gent, Gent University, De Pintelaan 185, 9000 Gent, Belgium. ; Gynaecologische Oncologie, KU Leuven, Herestraat 49, 3000 Leuven, Belgium. ; Laboratory of Computational Biology, Center for Human Genetics, KULeuven, Herestraat 49, 3000 Leuven, Belgium. ; Department of Applied Mathematics, Computer Science and Statistics, Gent University, De Pintelaan 185, 9000 Gent, Belgium. ; Department of Mathematics, KU Leuven, Celestijnenlann 200B, 3001 Leuven, Belgium. ; RNA Molecular Biology, Center for Microscopy and Molecular Imaging, Universite Libre de Bruxelles (ULB), rue des Professeurs Jeener et Brachet 12, 6041 Charleroi, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27008969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenesis/genetics/pathology ; Cell Lineage ; Cell Proliferation ; Cell Survival ; Chromosomes, Human, Pair 3/genetics ; Clone Cells/metabolism/pathology ; Female ; Gene Amplification/genetics ; Gene Knockdown Techniques ; Humans ; Melanoma/*genetics/*pathology/therapy ; Mice ; Microphthalmia-Associated Transcription Factor/genetics ; Mitochondria/genetics/metabolism/pathology ; Mitochondrial Proteins/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Molecular Targeted Therapy ; Oncogenes/*genetics ; RNA, Long Noncoding/*genetics/therapeutic use ; SOXE Transcription Factors/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    ISSN: 1617-4623
    Keywords: Key words Gene cloning ; Protein secretion ; Filamentous fungi ; Small GTP binding protein ; Complementation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The Aspergillusniger and Trichodermareesei genes encoding the functional homologues of the small GTP-binding protein SAR1p, which is involved in the secretion pathway in Saccharomyces cerevisiae, have been cloned and characterised. The A. niger gene (sarA) contains five introns, whereas the T. reesei gene (sar1) has only four. In both cases the first intron is at the same position as the single S. cerevisiae SAR1 intron. The encoded proteins show 70–80% identity to the SAR1 protein. Complementation of S. cerevisiaesar1 and sec12 mutants by expression vectors carrying the A. nigersarA and T. reesei sar1 cDNA clones confirmed that the cloned genes are functional homologues of the S. cerevisiae SAR1 gene. Three mutant alleles of the A. nigersarA gene (D29G, E109K, D29G/E109K), generated by site-directed mutagenesis, revealed a thermosensitive dominant-negative phenotype in the presence of the wild-type sarA allele. This result contrasts with the situation in S. cerevisiae, where similar mutations have a thermosensitive phenotype. Taken together, our results indicate that the sarA gene is involved in an essential function in A. niger.
    Type of Medium: Electronic Resource
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  • 4
  • 5
    Publication Date: 2014-12-16
    Description: Modern molecular genetics studies necessitate the manipulation of genes in their endogenous locus, but most of the current methodologies require an inefficient donor-dependent homologous recombination step to locally modify the genome. Here we describe a methodology to efficiently generate Drosophila knock-in alleles by capitalizing on the availability of numerous genomic MiMIC transposon insertions carrying recombinogenic attP sites. Our methodology entails the efficient PhiC31-mediated integration of a recombination cassette flanked by unique I-SceI and/or I-CreI restriction enzyme sites into an attP -site. These restriction enzyme sites allow for double-strand break–mediated removal of unwanted flanking transposon sequences, while leaving the desired genomic modifications or recombination cassettes. As a proof-of-principle, we mutated LRRK , tau , and sky by using different MiMIC elements. We replaced 6 kb of genomic DNA encompassing the tau locus and 35 kb encompassing the sky locus with a recombination cassette that permits easy integration of DNA at these loci and we also generated a functional LRRK HA knock in allele. Given that ~92% of the Drosophila genes are located within the vicinity (〈35 kb) of a MiMIC element, our methodology enables the efficient manipulation of nearly every locus in the fruit fly genome without the need for inefficient donor-dependent homologous recombination events.
    Electronic ISSN: 2160-1836
    Topics: Biology
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  • 6
    Publication Date: 2006-10-01
    Print ISSN: 0168-9525
    Electronic ISSN: 1362-4555
    Topics: Biology
    Published by Cell Press
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  • 7
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