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. 2008 Jul 15;105(29):9936–9941. doi: 10.1073/pnas.0804510105

Fig. 3.

Fig. 3.

Replication stalling at the inverted Alu repeats depends on the level of sequence homology and is independent of the presence of the SbcC nuclease. (A) 2D gels showing replication through Alu IRs with different degrees of sequence homology in E. coli and COS-1 cells. (B) Quantitative analysis of the replication stalling caused by Alu IRs with various sequence divergence. ◆, E. coli; □, COS-1 cells. (C) Replication fork stalling at Alu IRs with 86% homology in the WT and sbcC− E. coli strains.