Replication factor C complexes play unique pro- and anti-establishment roles in sister chromatid cohesion.
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.
Department of Biological Sciences, Lehigh University, Bethlehem, Pennsylvania, United States of America.
Marie E
ME
Maradeo
Robert V
RV
Skibbens
D000107:Acetylation; D001483:Base Sequence; D017931:DNA Primers; D005434:Flow Cytometry; D055786:Gene Knockout Techniques; D009154:Mutation; D018809:Proliferating Cell Nuclear Antigen / Q000502:physiology; D051818:Replication Protein C / Q000502:physiology*; D012854:Sister Chromatid Exchange
D017931:DNA Primers; D018809:Proliferating Cell Nuclear Antigen; D051818:Replication Protein C