IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_ncomms15025.html
   My bibliography  Save this article

PIF1 family DNA helicases suppress R-loop mediated genome instability at tRNA genes

Author

Listed:
  • Phong Lan Thao Tran

    (Lewis Thomas Laboratory, Princeton University)

  • Thomas J. Pohl

    (Lewis Thomas Laboratory, Princeton University)

  • Chi-Fu Chen

    (Lewis Thomas Laboratory, Princeton University)

  • Angela Chan

    (Lewis Thomas Laboratory, Princeton University)

  • Sebastian Pott

    (University of Chicago)

  • Virginia A. Zakian

    (Lewis Thomas Laboratory, Princeton University)

Abstract

Saccharomyces cerevisiae encodes two Pif1 family DNA helicases, Pif1 and Rrm3. Rrm3 promotes DNA replication past stable protein complexes at tRNA genes (tDNAs). We identify a new role for the Pif1 helicase: promotion of replication and suppression of DNA damage at tDNAs. Pif1 binds multiple tDNAs, and this binding is higher in rrm3Δ cells. Accumulation of replication intermediates and DNA damage at tDNAs is higher in pif1Δ rrm3Δ than in rrm3Δ cells. DNA damage at tDNAs in the absence of these helicases is suppressed by destabilizing R-loops while Pif1 and Rrm3 binding to tDNAs is increased upon R-loop stabilization. We propose that Rrm3 and Pif1 promote genome stability at tDNAs by displacing the stable multi-protein transcription complex and by removing R-loops. Thus, we identify tDNAs as a new source of R-loop-mediated DNA damage. Given their large number and high transcription rate, tDNAs may be a potent source of genome instability.

Suggested Citation

  • Phong Lan Thao Tran & Thomas J. Pohl & Chi-Fu Chen & Angela Chan & Sebastian Pott & Virginia A. Zakian, 2017. "PIF1 family DNA helicases suppress R-loop mediated genome instability at tRNA genes," Nature Communications, Nature, vol. 8(1), pages 1-10, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15025
    DOI: 10.1038/ncomms15025
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms15025
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms15025?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15025. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.