Stalled forks

Replication fork stalling occurs if the replication proteins, or replisome, encounter problems. Stalled forks activate checkpoint signalling and therefore pause replication.

Latest Research and Reviews

  • Research |

    BRCA1–BARD1 has a role in replication fork protection that is mediated by a mechanism of phosphorylation-targeted isomerization of BRCA1 and is independent of the canonical interaction between BRCA1 and PALB2.

    • Manuel Daza-Martin
    • , Katarzyna Starowicz
    • , Mohammed Jamshad
    • , Stephanie Tye
    • , George E. Ronson
    • , Hannah L. MacKay
    • , Anoop Singh Chauhan
    • , Alexandra K. Walker
    • , Helen R. Stone
    • , James F. J. Beesley
    • , Jennifer L. Coles
    • , Alexander J. Garvin
    • , Grant S. Stewart
    • , Thomas J. McCorvie
    • , Xiaodong Zhang
    • , Ruth M. Densham
    •  & Joanna R. Morris
    Nature, 1-7
  • Reviews |

    The choice between the major DNA double-strand break repair pathways is important for maintaining genomic stability. In mammals, selecting one pathway over another involves a complex series of binary ‘decisions’. Emerging evidence suggests that the ‘decision tree’ governing repair-pathway choice at stalled replication forks differs from that of replication-independent double-strand breaks.

    • Ralph Scully
    • , Arvind Panday
    • , Rajula Elango
    •  & Nicholas A. Willis
  • Research | | open

    Measuring relative frequencies of DNA double-strand breaks between loci does not provide the full physiological relevance of those breaks. Here Rowicka and colleagues present qDSB-Seq method which uses spike-in double-strand breaks induced by a restriction enzyme to accurately quantify DNA damage.

    • Yingjie Zhu
    • , Anna Biernacka
    • , Benjamin Pardo
    • , Norbert Dojer
    • , Romain Forey
    • , Magdalena Skrzypczak
    • , Bernard Fongang
    • , Jules Nde
    • , Razie Yousefi
    • , Philippe Pasero
    • , Krzysztof Ginalski
    •  & Maga Rowicka
  • Research | | open

    Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their checkpoint function.

    • Julien N. Bianco
    • , Valérie Bergoglio
    • , Yea-Lih Lin
    • , Marie-Jeanne Pillaire
    • , Anne-Lyne Schmitz
    • , Julia Gilhodes
    • , Amelie Lusque
    • , Julien Mazières
    • , Magali Lacroix-Triki
    • , Theodoros I. Roumeliotis
    • , Jyoti Choudhary
    • , Jérôme Moreaux
    • , Jean-Sébastien Hoffmann
    • , Hélène Tourrière
    •  & Philippe Pasero

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