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. 2013 May 6;110(21):E1963–E1971. doi: 10.1073/pnas.1221347110

Fig. 3.

Fig. 3.

The role of ABA in defense against TMC-cg infection. (A) Expression of ABA1, ABA2, and ABA3 in wild-type leaves systemically infected by TMV-cg at 3, 5, and 7 dpi. (B) Expression of ABI4 in wild-type leaves systemically infected by TMV-cg at 3, 5, and 7 dpi. (C) Expression of ABI4 in wild-type and wrky8 leaves systemically infected by TMV-cg at 6 dpi. (D) ABA delays the accumulation of TMV-cg in systemically infected leaves. Three leaves of 26-d-old wild-type plants treated or not treated with 100 µM ABA were inoculated with TMV-cg. Leaf collection, RNA isolation, and RNA blot analysis of TMV-cg CP were performed as in Fig. 1. (E) Mutation of abi4, aba1, aba2, or aba3 promotes the accumulation of TMV-cg in systemically infected leaves. Inoculation, leaf collection, RNA isolation, and RNA blot analysis of TMV-cg CP were performed as in Fig. 1. These experiments were repeated three times with similar results.