Priority Research Paper Volume 12, Issue 18 pp 17761—17785

An ordered assembly of MYH glycosylase, SIRT6 protein deacetylase, and Rad9-Rad1-Hus1 checkpoint clamp at oxidatively damaged telomeres

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Figure 7. Models for response of SIRT6, MYH, and Rad9-Rad1-Hus1 to repair DNA damages on damaged telomeres. SIRT6, MYH, and Rad9-Rad1-Hus1 form a repair complex in a cooperative manner. (A) SIRT6 is recruited to damage telomeres at a very early step and then recruits MYH and Hus1 following oxidative stress. However, 30% of Hus1 can also respond to damaged telomeres independently on SIRT6. (B) A weaker interaction between MYH and Hus1 in the sirt6-/- cells leads to the loss of association of MYH at damaged telomeres. (C) A weaker interaction between MYH and SIRT6 in the hus1-/- cells leads to the loss of association of MYH at damaged telomeres. (D) A weaker interaction between Hus1 and SIRT6 in the MYH KO cells reduces the SIRT6-dependent 9-1-1 association but does not affect the SIRT6-independent 9-1-1 association at damaged telomeres.