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Hirokazu Tanaka^1,, Yuki Katou^1,, Masaru Yagura², Katsuya Saitoh¹, Takehiko Itoh³, Hiroyuki Araki², Masashige Bando¹ and Katsuhiko Shirahige¹

¹ Laboratory of Chromosome Structure and Function, Department of Biological Science, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, B-20, 4259, Nagatsuta, Midori-ku, Yokohama City, Kanagawa 226-8501, Japan
² Division of Microbial Genetics, National Institute of Genetics, Research Organization of Information and Systems, Sokendai, Yata 1111, Mishima, Shizuoka 411-8540, Japan
³ Research Center for Advanced Science and Technology, Mitsubishi Research Institute Inc., Chiyoda-ku, Tokyo, Japan

Ctf4 is a protein conserved in eukaryotes and a constituent of the replisome progression complex. It also plays a role in the establishment of sister chromatid cohesion. In our current study, we demonstrate that the replication checkpoint is activated in the absence of Ctf4, and that the interaction between the MCM helicase-go ichi ni san (GINS) complex and DNA polymerase (Pol )-primase is destabilized specifically in a ctf4 mutant. An in vitro interaction between GINS and DNA Pol was also found to be mediated by Ctf4. The same interaction was not affected in the absence of the replication checkpoint mediators Tof1 or Mrc1. In ctf4 cells, DNA pol became significantly unstable and was barely detectable at the replication forks in HU. In contrast, the quantities of helicase and DNA pol bound to replication forks were almost unchanged but their localizations were widely and abnormally dispersed in the mutant cells compared with wild type. These results lead us to propose that Ctf4 is a key connector between DNA helicase and Pol and is required for the coordinated progression of the replisome.

These two authors contributed equally to this work.

^* Correspondence: mbando{at}bio.titech.ac.jp or kshirahi{at}bio.titech.ac.jp

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