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. Author manuscript; available in PMC: 2013 Apr 26.
Published in final edited form as: Cell. 2012 Oct 26;151(3):497–507. doi: 10.1016/j.cell.2012.09.033

Figure 5. Effect of the C377G mutation on group II intron splicing.

Figure 5

Wild type O.i. group II intron splices efficiently under physiological K+ concentrations, while the C377G mutant has an evident splicing defect and accumulates intermediate product (I-3e, red and blue boxes, respectively). Specifically, the rate constants of the C377G mutant are reduced by ~11-fold in the first step and by ~37-fold in the second step of splicing with respect to wild type, respectively (Table S4). The graph on the right shows the evolution of the population of intermediate over time. The error bars represent the standard deviation calculated from three independent experiments. Intermediate (I3e) and linear intron (I) migrate as double bands because of cryptic cleavage at nucleotides (−11) and (−10) from the 5′-end of the intron, as explained in Extended Experimental Procedures. See also Figure S5.