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. 2012 May 15;23(10):1943–1954. doi: 10.1091/mbc.E11-10-0829

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© 2012 Barkley et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 6: — Hypothetical model showing roles of DDK and JNK in UV-inducible Rad18 phosphorylation and DNA damage tolerance. UV induces JNK-mediated phosphorylation of S409 and DDK-mediated phosphorylation of the S-box serine cluster. UV-induced phosphorylation of both S409 and the S-box is Chk1 dependent (step 1). S409 and the S-box reside in the Polη-binding region of Rad18 (residues 401–445). S409 and S-box phosphorylations promote Rad18–Polη interactions (step 2), thereby facilitating Rad18-dependent chaperoning of Polη to sites of replication stalling, where the Rad18–Polη complex associates with RPA-coated ssDNA (step 3).