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

Fig. 5.

Fig. 5.

The role of ET in defense against TMC-cg infection. (A) Expression of ACS6 in wild-type leaves systemically infected dpi by TMV-cg at 3, 4, 5, 6, and 7. (B) Expression of ERF104 in wild-type leaves systemically infected by TMV-cg at 3, 4, 5, 6, and 7 dpi. (C) ACC promotes 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 ACC were inoculated with TMV-cg. Leaf collection, RNA isolation, and RNA blot analysis of TMV-cg CP were performed as in Fig. 1. (D) Mutation of acs6 or erf104 inhibits 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. (E) Mutation of eight acs genes (acs1/2/4/5/6/7/9/11) or ein2 inhibits 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 at least twice with similar results.