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. 2016 Mar 18;12(3):e1005942. doi: 10.1371/journal.pgen.1005942

Fig 6. Proposed molecular mechanism for promoting imprecise end joining in the xrs2 FHA mutants.

Fig 6

A. DSB repair process in xrs2 FHA mutants. Compromised Tel1 activity causes accumulation or persistent localization of Ku at processed DSB ends, which then often facilitates Ku-dependent imprecise end joining. B. Tel1 is recruited to DSB ends in a manner dependent on Xrs2 Tel1-binding domain. C. Then, robust activation of Tel1 is promoted in an Xrs2 FHA-dependent manner. The color change and halo effect of Tel1 indicates relative amounts of Tel1 activation. D. Phosphorylation of Sae2 or other unknown factors by Tel1 and/or Mec1 plays a role in DSB end resection as well as Ku removal to promote HR.