When a specific part of a plant is attacked by a fungal pathogen, distant parts of the plant may display an enhanced state of resistance involving the accumulation of pathogenesis-related (PR) proteins, a class of plant proteins that are normally not present but that are induced upon pathogen attack (reviewed by Van Loon and Van Strien, 1999). In addition, salicylic acid (SA; 6.28) and hydrogen peroxide accumulate at the wound site and in other parts of the plant. This response is referred to as systemic acquired resistance (SAR) and is thought to be mediated by one or more signaling molecules in the phloem.
SA was hypothesized to be one of those signaling molecules, because 1) SA accumulation was shown to be correlated with SAR and resistance (Uknes et al., 1993), 2) exogenous SA applied to an uninfected plant induced SAR and resistance in a manner similar to that of an infected plant (Ward et al., 1991), and 3) transgenic plants expression the nahG gene from Pseudomonas putida, which encodes a salicilate hydroxylase, were unable to display SAR (Gaffney et al., 1993).
SA was hypothesized to be one of those signaling molecules, because 1) SA accumulation was shown to be correlated with SAR and resistance (Uknes et al., 1993), 2) exogenous SA applied to an uninfected plant induced SAR and resistance in a manner similar to that of an infected plant (Ward et al., 1991), and 3) transgenic plants expression the nahG gene from Pseudomonas putida, which encodes a salicilate hydroxylase, were unable to display SAR (Gaffney et al., 1993). While this latter study demonstrated the role of SA in initiating SAR, it did not address whether SA was the signaling molecule that transmitted the SAR signal through the phloem to other parts of the plant. Vernooij et al. (1994) performed a series of elegant experiments to investigate the role of SA in signaling. They grafted a scion from a transgenic tobacco plant expressing the NahG gene onto the root stock of an untransformed tobacco plant. In addition, an untransformed scion was grafted onto a transgenic rootstock. Ungrafted plants and plants where the scion was grafted back on the rootstock from which it came were used as controls. The root stocks were inoculated with the viral pathogen tobacco mosaic virus (TMV) to induce SAR. The degree of SAR was evaluated by challenging the scions of the inoculated plants 7 days later with TMV or the fungal pathogen Cercospora nicotianae. In the untransformed graft control, the lesions induced by TMV were 41% smaller compared to a mock-inoculated control. This indicated that the SAR signal was not hampered by the graft. When the scions of the transgenic grafted plants were inoculated, the lesion size was the same as in the corresponding mock-inoculated control. This indicated that the expression of the NahG gene prevented SAR, as had been shown by Gaffney et al. (1993). The TMV-inoculated transgenic scions on untransformed root stocks behaved similarly as the mock-inoculated controls, indicating that SA was required to induce SAR in the scions. When untransformed scions on transgenic root stocks were inoculated with TMV, however, they displayed SAR. This reveals that the NahG-expressing tissues were able to transmit the signal required for
SAR. Similar results were obtained when the SAR response was induced by C. nicotianae, suggesting that SAR is a response to a broad range of pathogens. These experiments thus demonstrated that SA is required for the induction of SAR, but that it is not the actual signaling molecule.
After an additional 10 years of research it is still not entirely clear what the signaling molecule is. Van Bel and Gaupels (2004) recently reviewed the possible signaling molecules that could induce SAR. The list includes jasmonic acid, lipid-derived molecules, reactive oxygen species (see Chapter 2, Section 1.9), oligosaccharides, mRNA molecules, calcium, and various peptides.
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