Yeast Rad5 Protein Required for Postreplication Repair Has a DNA Helicase Activity Specific for Replication Fork Regression

András Blastyák, Lajos Pintér, Ildiko Unk, Louise Prakash, Satya Prakash, Lajos Haracska

Research output: Contribution to journalArticle

199 Scopus citations


Lesions in the template DNA strand block the progression of the replication fork. In the yeast Saccharomyces cerevisiae, replication through DNA lesions is mediated by different Rad6-Rad18-dependent means, which include translesion synthesis and a Rad5-dependent postreplicational repair pathway that repairs the discontinuities that form in the DNA synthesized from damaged templates. Although translesion synthesis is well characterized, little is known about the mechanisms that modulate Rad5-dependent postreplicational repair. Here we show that yeast Rad5 has a DNA helicase activity that is specialized for replication fork regression. On model replication fork structures, Rad5 concertedly unwinds and anneals the nascent and the parental strands without exposing extended single-stranded regions. These observations provide insight into the mechanism of postreplicational repair in which Rad5 action promotes template switching for error-free damage bypass.

Original languageEnglish (US)
Pages (from-to)167-175
Number of pages9
JournalMolecular cell
Issue number1
StatePublished - Oct 12 2007



  • DNA

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this