The Rad53 checkpoint function of Rad9 is not required for GCR suppression and growth in the presence of MMS in cells lacking Sgs1.

<p>(<b>A</b>) Illustration of the domain structure of Rad9. (<b>B</b>) Immunoprecipitations were conducted with extracts from the contructed <i>rad9 ^7xA-</i>HA strain (LBy-471) and the <i>sgs1Δrad9 ^7xA</i>-HA strain (LBy-472) to verify the 7xA mutations. Immunoprecipitations were performed with anti-HA antibody in the presence and absence of MMS. (<b>C</b>) Survival was monitored as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081015#s2" target="_blank">Materials and Methods</a> after 70 min exposure to different concentrations of MMS for the indicated strains: wild type (LBy-1), <i>sgs1Δ</i> (LBy-129), <i>rad9Δ</i> (LBy-316), <i>sgs1Δrad9Δ</i> (LBy-44), <i>rad9 ^7xA</i> (LBy-471), <i>sgs1Δ rad9 ^7xA</i> (LBy-472). (<b>D</b>) GCR were measured after exposure to 0.02% MMS and is shown as fold increase over wild type for the isogenic strains: <i>sgs1Δ</i> (LBy-388), <i>rad24Δ</i> (LBy-406), <i>rad9Δ</i> (LBy-389), <i>rad9 ^7xA</i> (LBy-473), <i>sgs1Δ rad9 ^7xA</i> (LBy-474).