Having previously shown that the MTC complex greatly stimulates progression of the leading strand replisome even in the absence of Mcm10 (Figure 4), we tested the MTC complex in CMG helicase assays to see if it enhances the ability of CMG to bypass blocks on DNA (Figure 5C). In contrast to Mcm10, MTC was unable to promote CMG bypass of the block (compare lanes 11–13 in Figure 5C to lanes 11–13 in Figure 5B). We also note that MTC did not stimulate CMG unwinding even in the absence of the block (Figure 5C compare lanes 8–10 with MTC to lanes 2–4 without MTC), suggesting that MTC does not function at the level of CMG unwinding. Together with the results of Figures 2–4, these data suggest that Mcm10 and MTC affect fork progression in very different ways. In contrast to Mcm10 mediated bypass of lagging strand blocks, CMG unwinding was delayed and strongly repressed by a dual streptavidin block on the leading strand even with Mcm10 present (Figure 5—figure supplement 1).