Replication factor C complexes play unique pro- and anti-establishment roles in sister chromatid cohesion

PLoS One. 2010 Oct 27;5(10):e15381. doi: 10.1371/journal.pone.0015381.

Abstract

Recent studies have lead to a rapid expansion of sister chromatid cohesion pathways. Of particular interest is the growth in classifications of anti-establishment factors-now including those that are cohesin-associated (Rad61/WAPL and Pds5) or DNA replication fork-associated (Elg1-RFC). In this study, we show that the two classes of anti-establishment complexes are indistinguishable when challenged both genetically and functionally. These findings suggest that both classes function in a singular pathway that is centered on Ctf7/Eco1 (herein termed Ctf7) regulation. The anti-establishment activity of Elg1-RFC complex is particular intriguing given that an alternate Ctf18-RFC complex exhibits robust pro-establishment activity. Here, we provide several lines of evidence, including the use of Ctf7 bypass suppressors, indicating that these activities are not simply antagonistic. Moreover, the results suggest that Ctf18-RFC is capable of promoting sister chromatid pairing reactions independent of Ctf7. The combination of these studies suggest a new model of sister chromatid pairing regulation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Base Sequence
  • DNA Primers
  • Flow Cytometry
  • Gene Knockout Techniques
  • Mutation
  • Proliferating Cell Nuclear Antigen / physiology
  • Replication Protein C / physiology*
  • Sister Chromatid Exchange*

Substances

  • DNA Primers
  • Proliferating Cell Nuclear Antigen
  • Replication Protein C