The Slx4-Dpb11 scaffold complex: coordinating the response to replication fork stalling in S-phase and the subsequent mitosis
作者： Lissa N Princz , Dalia Gritenaite , Boris Pfander
DOI: 10.4161/15384101.2014.989126
关键词:
摘要: Replication fork stalling at DNA lesions is a common problem during the process of replication. One way to allow bypass these via specific recombination-based mechanisms that involve switching replication template sister chromatid. Inherent formation joint molecules (JMs) between chromatids. Such JMs need be disentangled before chromatid separation in mitosis and activity JM resolution enzymes, which under stringent cell cycle control, therefore up-regulated mitosis. An additional layer control facilitated by scaffold proteins. In budding yeast, specifically mitosis, Slx4 Dpb11 form kinase-dependent complex with Mus81-Mms4 structure-selective endonuclease, allows efficient Mus81. Furthermore, interact even prior joining Mus81 respond S-phase. This S-phase involved regulation damage checkpoint as well early steps switch recombination. Similar interactions regulatory principles are found human cells suggesting may have an evolutionary conserved role organizing cellular response stalling.
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