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      Pif1 family helicases suppress genome instability at G-quadruplex motifs

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          Abstract

          The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans. We show that exceptionally potent G-quadruplex unwinding is conserved amongst Pif1 helicases. Moreover, Pif1 helicases from organisms separated by >3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast. The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to novel genetic and epigenetic changes. Further, when expressed in yeast, human Pif1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.

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          A second set of loxP marker cassettes for Cre-mediated multiple gene knockouts in budding yeast.

          U Gueldener (2002)
          Heterologous markers are important tools required for the molecular dissection of gene function in many organisms, including Saccharomyces cerevisiae. Moreover, the presence of gene families and isoenzymes often makes it necessary to delete more than one gene. We recently introduced a new and efficient gene disruption cassette for repeated use in budding yeast, which combines the heterologous dominant kan(r) resistance marker with a Cre/loxP-mediated marker removal procedure. Here we describe an additional set of four completely heterologous loxP-flanked marker cassettes carrying the genes URA3 and LEU2 from Kluyveromyces lactis, his5(+) from Schizosaccharomyces pombe and the dominant resistance marker ble(r) from the bacterial transposon Tn5, which confers resistance to the antibiotic phleomycin. All five loxP--marker gene--loxP gene disruption cassettes can be generated using the same pair of oligonucleotides and all can be used for gene disruption with high efficiency. For marker rescue we have created three additional Cre expression vectors carrying HIS3, TRP1 or ble(r) as the yeast selection marker. The set of disruption cassettes and Cre expression plasmids described here represents a significant further development of the marker rescue system, which is ideally suited to functional analysis of the yeast genome.
          Article 0 comments Cited 332 times – based on 0 reviews     Review now
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            DNA replication through G-quadruplex motifs is promoted by the Saccharomyces cerevisiae Pif1 DNA helicase.

            Katrin Paeschke, John A Capra, Virginia Zakian (2011)
            G-quadruplex (G4) DNA structures are extremely stable four-stranded secondary structures held together by noncanonical G-G base pairs. Genome-wide chromatin immunoprecipitation was used to determine the in vivo binding sites of the multifunctional Saccharomyces cerevisiae Pif1 DNA helicase, a potent unwinder of G4 structures in vitro. G4 motifs were a significant subset of the high-confidence Pif1-binding sites. Replication slowed in the vicinity of these motifs, and they were prone to breakage in Pif1-deficient cells, whereas non-G4 Pif1-binding sites did not show this behavior. Introducing many copies of G4 motifs caused slow growth in replication-stressed Pif1-deficient cells, which was relieved by spontaneous mutations that eliminated their ability to form G4 structures, bind Pif1, slow DNA replication, and stimulate DNA breakage. These data suggest that G4 structures form in vivo and that they are resolved by Pif1 to prevent replication fork stalling and DNA breakage. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Position effect at S. cerevisiae telomeres: reversible repression of Pol II transcription.

              D Gottschling, O M Aparicio, B Billington … (1990)
              S. cerevisiae chromosomes end with the telomeric repeat (TG1-3)n. When any of four Pol II genes was placed immediately adjacent to the telomeric repeats, expression of the gene was reversibly repressed as demonstrated by phenotype and mRNA analyses. For example, cells bearing a telomere-linked copy of ADE2 produced predominantly red colonies (a phenotype characteristic of ade2- cells) containing white sectors (characteristic of ADE2+ cells). Repression was due to proximity to the telomere itself since an 81 bp tract of (TG1-3)n positioned downstream of URA3 when URA3 was approximately 20 kb from the end of chromosome VII did not alter expression of the gene. However, this internal tract of (TG1-3)n could spontaneously become telomeric, in which case expression of the URA3 gene was repressed. These data demonstrate that yeast telomeres exert a position effect on the transcription of nearby genes, an effect that is under epigenetic control.
              Article 0 comments Cited 200 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0410462
                Journal ID (pubmed-jr-id): 6011
                Journal ID (nlm-ta): Nature
                Journal ID (iso-abbrev): Nature
                Title: Nature
                ISSN (Print): 0028-0836
                ISSN (Electronic): 1476-4687
                Publication date Nihms-submitted: 31 May 2013
                Publication date (Electronic): 08 May 2013
                Publication date (Print): 23 May 2013
                Publication date PMC-release: 23 November 2013
                Volume: 497
                Issue: 7450
                Pages: 458-462
                Affiliations
                [1 ]Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
                [2 ]Departments of Microbiology and Molecular and Cellular Biology, University of California, Davis, CA 95616, USA
                [3 ]Department of Biological Sciences, Vanderbilt University, Nashville, TN 37232, USA
                Author notes
                Correspondence and requests for materials should be addressed to V.A.Z. ( vzakian@ 123456princeton.edu )
                [*]

                These authors contributed equally to this work.

                [†]

                Current address: Department of Biochemistry, Theodor Boveri-Institute, University of Würzburg, Am Hubland, D-97074 Würzburg, Germany.

                [‡]

                Current address: Institute of Molecular Cancer Research, University of Zurich, Winterthurerstrasse 190, Zurich 8057, Switzerland.

                Article
                Manuscript ID: NIHMS464886
                DOI: 10.1038/nature12149
                PMC ID: 3680789
                PubMed ID: 23657261
                SO-VID: 090b0da0-5878-4ef6-9ca0-17c74ce22faa
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Institute of General Medical Sciences : NIGMS
                Award ID: R01 GM043265 || GM
                Funded by: National Institute of General Medical Sciences : NIGMS
                Award ID: R01 GM026938 || GM
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                Subject: Article

                ScienceOpen disciplines: Uncategorized
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