Do the enzyme PAL and Peroxidase is characteristic for induced resistance toward the pathogens, and how I can measured it in the plant tissue
PAL, PPO, POD all are defense enzymes produced when the host plant is induced by either biotic or abiotic agents. Thousands of research articles available online.Please search.
PAL and Peroxidase are induced by biotic and abiotic agents. Sometimes such induction is related to resistance (e.g. lignification, phytoalexin biosynthesis, etc.). In other cases the indiction is a way to alleviate the effects of the stress, (e.g. removing H2O2 in the case of peroxidase). A good review about peroxidases in plant pathogen interactions is Almagro et al. 2009. J. Exp. Bot. 60 (2): 377-390.
I want to make a small clarification.
Activation of PAL associated with the accumulation of salicylic acid. The activation of POX bind with the accumulation of lignin. Accordingly, the individual activation of the PAL could be closely related to the launch of the system on the defence with salicylic acid. At the same time, the salicylic acid can effectively utilized as a substrate of POX for formation of lignin. However, in the latter case, it is necessary to look at activation of individual POX isoenzymes. Part of its is induced by salicylic acid and part with jasmonic acid. Reviews are many, but the subtle nuances of the enzymes are not yet disclosed
It is true that PAL could be associated to salicylic acid (SA) biosynthesis. However, PAL is also related to the biosynthesis of phenolic phytoalexins and lignin monomers. Moreover, the PAL pathway is not the only one for SA biosynthesis: there is also the Isochorismate pathway, independent from PAL. Therefore, PAL induction not always point to SA accumulation.
I agree with that, but the second does not exclude the former.
In addition there is also the way the release of salicylic acid from the binding forms.
I think that in some cases we can talk about the involvement of the PAL and some apoplastic isoenzymes PRX, for example, capable of binding to the cell wall of pathogens, in systemic and local defense mechanisms.
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