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. 2007 Apr 1;21(7):821–834. doi: 10.1101/gad.1536107

Figure 3.

Figure 3.

Disrupting U2 stem IIc or flanking structures mutually exclusive with stem IIa suppresses a mutation in PRP16, a DExD/H box ATPase. (A,B) Disruption of U2 stem IIc suppresses the mutation prp16-302. Compensatory analysis by growth of the U2 stem IIc base pairs C59/G100 (A) and U56/A103 (B) in a wild-type PRP16 (left) or a mutant prp16-302 (right) strain is shown. The cells were grown for 3 d (left) or 6 d (right) at 20°C on solid media containing 5-FOA. (C,D) Disruption of structures mutually exclusive with stem IIa suppresses prp16-302. Compensatory analysis by growth of the U2 stem IIa base pairs G53/C62 (C) and A52/U63 (D) in a wild-type PRP16 (left) or a mutant prp16-302 (right) strain. Cells were grown for 3 d (D, left), 4 d (C, left) or 6 d (C,D, right) at 20°C on solid media containing 5-FOA. Black boxes indicate that the mutation is lethal and could not be tested. Matrices are labeled as in Figure 1.