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  • 1
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    Meiosis. Searching for a partner (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, J E -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):823-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel Center, Department of Biology, Brandeis University, Waltham, MA 02254-9110, USA. haber@hydra.rose.brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9480551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/physiology ; Crossing Over, Genetic ; DNA/metabolism ; DNA, Fungal/metabolism ; Drosophila/genetics/*physiology ; Gene Conversion ; *Meiosis ; *Recombination, Genetic ; Saccharomyces/genetics/*physiology ; Synaptonemal Complex/*physiology
    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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  • 2
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    Removal of nonhomologous DNA ends in double-strand break recombination: the role of the yeast ultraviolet repair gene RAD1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-16
    Description: Double-strand breaks (DSBs) in Saccharomyces cerevisiae can be repaired by gene conversions or by deletions resulting from single-strand annealing between direct repeats of homologous sequences. Although rad1 mutants are resistant to x-rays and can complete DSB-mediated mating-type switching, they could not complete recombination when the ends of the break contained approximately 60 base pairs of nonhomology. Recombination was restored when the ends of the break were made homologous to donor sequences. Additionally, the absence of RAD1 led to the frequent appearance of a previously unobserved type of recombination product. These data suggest RAD1 is required to remove nonhomologous DNA from the 3' ends of recombining DNA, a process analogous to the excision of photodimers during repair of ultraviolet-damaged DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fishman-Lobell, J -- Haber, J E -- GM01722/GM/NIGMS NIH HHS/ -- GM20056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 16;258(5081):480-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411547" target="_blank"〉PubMed〈/a〉
    Keywords: *DNA Repair ; DNA, Fungal/genetics ; Deoxyribonucleases, Type II Site-Specific/*metabolism ; Gene Conversion ; Kinetics ; *Recombination, Genetic ; Saccharomyces cerevisiae/*genetics ; Saccharomyces cerevisiae Proteins ; Sequence Deletion ; Ultraviolet Rays
    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
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    Comment on "Cell type regulates selective segregation of mouse chromosome 7 DNA strands in mitosis" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Armakolas and Klar (Reports, 24 February 2006, p. 1146) suggested that segregation of mouse chromosome 7, after induction of a site-specific crossover between homologous chromosomes, is driven by a preferential inheritance of the old Watson and the old Crick DNA strands. However, this interpretation only considered half of the possible outcomes. The conjecture fails when all possible outcomes are examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, James E -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1045; author reply 1045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel Center and Department of Biology, Brandeis University, Waltham, MA 02454-9110, USA. haber@brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Chromatids/physiology ; *Chromosome Segregation ; Chromosomes, Mammalian/*physiology ; Crossing Over, Genetic ; DNA/metabolism ; Ectoderm/cytology ; Embryo, Mammalian/cytology ; Endoderm/cytology ; G2 Phase ; Mice ; *Mitosis ; Recombination, Genetic ; Stem Cells/cytology
    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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  • 4
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    Migrating bubble during break-induced replication drives conservative DNA synthesis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-13
    Description: The repair of chromosomal double strand breaks (DSBs) is crucial for the maintenance of genomic integrity. However, the repair of DSBs can also destabilize the genome by causing mutations and chromosomal rearrangements, the driving forces for carcinogenesis and hereditary diseases. Break-induced replication (BIR) is one of the DSB repair pathways that is highly prone to genetic instability. BIR proceeds by invasion of one broken end into a homologous DNA sequence followed by replication that can copy hundreds of kilobases of DNA from a donor molecule all the way through its telomere. The resulting repaired chromosome comes at a great cost to the cell, as BIR promotes mutagenesis, loss of heterozygosity, translocations, and copy number variations, all hallmarks of carcinogenesis. BIR uses most known replication proteins to copy large portions of DNA, similar to S-phase replication. It has therefore been suggested that BIR proceeds by semiconservative replication; however, the model of a bona fide, stable replication fork contradicts the known instabilities associated with BIR such as a 1,000-fold increase in mutation rate compared to normal replication. Here we demonstrate that in budding yeast the mechanism of replication during BIR is significantly different from S-phase replication, as it proceeds via an unusual bubble-like replication fork that results in conservative inheritance of the new genetic material. We provide evidence that this atypical mode of DNA replication, dependent on Pif1 helicase, is responsible for the marked increase in BIR-associated mutations. We propose that the BIR mode of synthesis presents a powerful mechanism that can initiate bursts of genetic instability in eukaryotes, including humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3804423/" 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/PMC3804423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saini, Natalie -- Ramakrishnan, Sreejith -- Elango, Rajula -- Ayyar, Sandeep -- Zhang, Yu -- Deem, Angela -- Ira, Grzegorz -- Haber, James E -- Lobachev, Kirill S -- Malkova, Anna -- GM080600/GM/NIGMS NIH HHS/ -- GM76020/GM/NIGMS NIH HHS/ -- R01 GM080600/GM/NIGMS NIH HHS/ -- R01GM082950/GM/NIGMS NIH HHS/ -- R01GM084242/GM/NIGMS NIH HHS/ -- R03 ES016434/ES/NIEHS NIH HHS/ -- R03ES016434/ES/NIEHS NIH HHS/ -- R37 GM020056/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Oct 17;502(7471):389-92. doi: 10.1038/nature12584. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025772" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Breakage ; *DNA Breaks, Double-Stranded ; DNA Helicases/metabolism ; DNA Repair/genetics ; DNA Replication/*genetics ; DNA, Fungal/*biosynthesis/genetics ; Genomic Instability/genetics ; Mutagenesis/genetics ; S Phase/genetics ; Saccharomyces cerevisiae/cytology/enzymology/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/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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  • 5
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    Anaphase onset before complete DNA replication with intact checkpoint responses (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-10
    Description: Cellular checkpoints prevent mitosis in the presence of stalled replication forks. Whether checkpoints also ensure the completion of DNA replication before mitosis is unknown. Here, we show that in yeast smc5-smc6 mutants, which are related to cohesin and condensin, replication is delayed, most significantly at natural replication-impeding loci like the ribosomal DNA gene cluster. In the absence of Smc5-Smc6, chromosome nondisjunction occurs as a consequence of mitotic entry with unfinished replication despite intact checkpoint responses. Eliminating processes that obstruct replication fork progression restores the temporal uncoupling between replication and segregation in smc5-smc6 mutants. We propose that the completion of replication is not under the surveillance of known checkpoints.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torres-Rosell, Jordi -- De Piccoli, Giacomo -- Cordon-Preciado, Violeta -- Farmer, Sarah -- Jarmuz, Adam -- Machin, Felix -- Pasero, Philippe -- Lisby, Michael -- Haber, James E -- Aragon, Luis -- GM 20056/GM/NIGMS NIH HHS/ -- MC_U120074328/Medical Research Council/United Kingdom -- R01 GM061766/GM/NIGMS NIH HHS/ -- R01 GM061766-07/GM/NIGMS NIH HHS/ -- R01 GM061766-08/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1411-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Cycle Group, Medical Research Council (MRC) Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347440" target="_blank"〉PubMed〈/a〉
    Keywords: *Anaphase ; Cell Cycle Proteins/genetics/metabolism ; Checkpoint Kinase 2 ; Chromosome Segregation ; Chromosomes, Fungal/*genetics/metabolism ; DNA Breaks, Double-Stranded ; DNA Damage ; *DNA Replication ; DNA, Fungal/genetics/metabolism ; DNA, Ribosomal/*genetics/metabolism ; Genes, Fungal ; Genes, rRNA ; Metaphase ; *Mitosis ; Models, Genetic ; Mutation ; Nondisjunction, Genetic ; Protein-Serine-Threonine Kinases/metabolism ; S Phase ; Saccharomyces cerevisiae/*cytology/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/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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  • 6
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    Increased mutagenesis and unique mutation signature associated with mitotic gene conversion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: To examine the fidelity of DNA synthesis during double-strand break (DSB) repair in Saccharomyces cerevisiae we studied gene conversion in which both strands of DNA are newly synthesized. The mutation rate increases up to 1400 times over spontaneous events, with a significantly different mutation signature. Especially prominent are microhomology-mediated template switches. Recombination-induced mutations are largely independent of mismatch repair, by DNA polymerases Polzeta, Poleta, and Pol32, but result from errors made by Poldelta and Polepsilon. These observations suggest that increased DSB frequencies in oncogene-activated mammalian cells may also increase the probability of acquiring mutations required for transition to a cancerous state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254764/" 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/PMC4254764/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hicks, Wade M -- Kim, Minlee -- Haber, James E -- GM007122/GM/NIGMS NIH HHS/ -- GM20056/GM/NIGMS NIH HHS/ -- R01 GM020056/GM/NIGMS NIH HHS/ -- R37 GM020056/GM/NIGMS NIH HHS/ -- T32 GM007122/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):82-5. doi: 10.1126/science.1191125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Rosenstiel Center, Brandeis University, Waltham, MA 02454-9110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595613" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *DNA Breaks, Double-Stranded ; DNA Mismatch Repair ; DNA Polymerase II/metabolism ; DNA Polymerase III/metabolism ; *DNA Repair ; DNA, Fungal/biosynthesis ; DNA-Directed DNA Polymerase/metabolism ; *Gene Conversion ; Genes, Fungal ; *Mitosis ; Molecular Sequence Data ; *Mutagenesis ; *Mutation ; Oncogenes ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/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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  • 7
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    Retrospective. Fred Sherman (1932-2013) (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liebman, Susan W -- Haber, James E -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1059. doi: 10.1126/science.1248055.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Illinois at Chicago, Chicago, IL, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288325" target="_blank"〉PubMed〈/a〉
    Keywords: Genetics/*history ; History, 20th Century ; History, 21st Century ; Saccharomyces cerevisiae/*genetics ; United States
    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
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    Break-induced replication repair of damaged forks induces genomic duplications in human cells (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: In budding yeast, one-ended DNA double-strand breaks (DSBs) and damaged replication forks are repaired by break-induced replication (BIR), a homologous recombination pathway that requires the Pol32 subunit of DNA polymerase delta. DNA replication stress is prevalent in cancer, but BIR has not been characterized in mammals. In a cyclin E overexpression model of DNA replication stress, POLD3, the human ortholog of POL32, was required for cell cycle progression and processive DNA synthesis. Segmental genomic duplications induced by cyclin E overexpression were also dependent on POLD3, as were BIR-mediated recombination events captured with a specialized DSB repair assay. We propose that BIR repairs damaged replication forks in mammals, accounting for the high frequency of genomic duplications in human cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047655/" 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/PMC4047655/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Costantino, Lorenzo -- Sotiriou, Sotirios K -- Rantala, Juha K -- Magin, Simon -- Mladenov, Emil -- Helleday, Thomas -- Haber, James E -- Iliakis, George -- Kallioniemi, Olli P -- Halazonetis, Thanos D -- R01 GM076020/GM/NIGMS NIH HHS/ -- R37 GM020056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):88-91. doi: 10.1126/science.1243211. Epub 2013 Dec 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Geneva, 1205 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24310611" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cyclin E/biosynthesis/genetics ; *DNA Breaks, Double-Stranded ; DNA Polymerase III/genetics/*physiology ; DNA Repair/*genetics ; DNA Replication/*genetics ; *Gene Duplication ; Humans ; Neoplasms/*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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  • 9
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    Lethal disruption of the yeast actin gene by integrative DNA transformation (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-07-23
    Description: A mutant allele of the chromosomal locus corresponding to the cloned actin gene of the yeast Saccharomyces cerevisiae has been constructed by DNA transformation with a hybrid plasmid which integrates into, and thereby disrupts, the protein-encoding sequences of the gene. In a diploid strain of yeast, disruption of the actin gene on one chromosome results in a mutation that segregates as a recessive lethal tightly linked to a selectable genetic marker on the integrated plasmid. The actin gene, therefore, must encode an essential function for yeast cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shortle, D -- Haber, J E -- Botstein, D -- GM18973/GM/NIGMS NIH HHS/ -- GM20056/GM/NIGMS NIH HHS/ -- GM21253/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1982 Jul 23;217(4557):371-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7046050" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*genetics/physiology ; Alleles ; Cloning, Molecular ; DNA, Fungal/genetics ; DNA, Recombinant ; Genes, Lethal ; Genes, Recessive ; Plasmids ; Recombination, Genetic ; Saccharomyces cerevisiae/*genetics ; Transformation, Genetic
    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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  • 10
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    Meiotic recombination in yeast: alteration by multiple heterozygosities (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-18
    Description: Although meiotic gene conversion has long been known to be accompanied by crossing-over, a direct test of the converse has not been possible. An experiment was designed to determine whether crossing-over is accompanied by gene conversion in Saccharomyces cerevisiae. Nine restriction site heterologies were introduced into a 9-kilobase chromosomal interval that exhibits 22 percent crossing-over. Of all the exchange events that occurred, at least 59 percent of meiotic crossovers are accompanied by gene conversion of one or more of the restriction site heterologies. The average gene conversion tract length was 1.5 kilobases. An unexpected result was that the introduction of as few as seven heterozygosities significantly altered the outcome of recombination events, reducing the frequency of crossovers by 50 percent and increasing the number of exceptional tetrads. This alteration results from a second recombination event induced by repair of heteroduplex DNA containing multiple mismatched base pairs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borts, R H -- Haber, J E -- GM29736/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 18;237(4821):1459-65.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2820060" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Repair ; DNA Replication ; DNA Restriction Enzymes/metabolism ; DNA, Fungal/analysis ; Heterozygote ; *Meiosis ; *Recombination, Genetic ; Saccharomyces cerevisiae/*genetics
    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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