Rev7 inhibits the ATPase activity of Rad50 without impacting its ability to bind ATP. (A), Rad50 binds [γ-32P]ATP in a dose-dependent manner. Lane 1, no protein. Lanes 2-7, reactions were performed with 0.1, 0.2, 0.4, 0.6, 0.8 and 1 µM of Rad50 and 400 pmol γ-32P]ATP. (B) Quantification of ATP binding by Rad50 as a function of its concentration. (C) ScRev7 does not affect the ability of Rad50 to bind ATP. Lane 1, Rad50 and 400 pmol γ-32P]ATP. Lanes 2-7, same as in lane 1, but with 0.5, 1, 2, 4, 5, and 6 µM of ScRev7, respectively. (D) Quantification of the effect of ScRev7 on ATP binding by Rad50. (E) ATPase activity of Rad50 as a function of its concentration. Reactions were performed in the absence (lane 1) or presence (lanes 2-9) of 0.05, 0.1, 0.2, 0.3, 0.5, 0.6, 0.8 and 1 µM of Rad50, respectively. (F) Quantification of Rad50 ATPase activity as a function of its concentration. (G) ScRev7 abrogates ATP hydrolysis catalyzed by Rad50. (H) ScRev7-C1 variant impedes ATP hydrolysis catalyzed by Rad50. In panels (G) and (H) lane 1 contained 400 pmol γ-32P]ATP; lane 2, same as in lane, but 2 µM ScRev7/ScRev7-C1 variant; lane 3, as in lane 1, but with 0.5 µM Rad50; lanes 4-9, as in lane 3, but with 0.5 µM Rad50 and 0.1, 0.3, 0.5, 1, 1.5 and 2 µM ScRev7/ScRev7-C1 variant, respectively. (I) Quantification of the inhibitory effect of ScRev7/ScRev7-C1 on ATP hydrolysis catalyzed by Rad50. The closed triangles on the top of gel images in panels (A), (C), (E), (G) and (H) represent increasing concentrations of Rad50, ScRev7 or ScRev7-C1. Error bars indicate SEM, and data are representative of three independent experiments.