Plant cell wall reinforcement in the disease-resistance response: molecular composition and regulation

Abstract

The disease-resistance response of plant cells is composed of a multitude of biochemical events, and the activation of one of these, the phenylpropanoid metabolism, is pivotal for the survival of cells under stress conditions. The basic features of this facet of the disease-resistance response are beginning to be unraveled in model plant cell culture systems. These studies revealed a novel, alternative pathway for the synthesis of cell wall bound hydroxycinnamoyl esters and lignin. The investigations have, therefore, set the stage for a detailed analysis of the induction process that includes fast, posttranslational activation mechanisms as well as de novo enzyme synthesis. The biosynthesis of phenolic compounds destined for the cell wall is considered to reach far beyond the mere physical strengthening of the cells and includes additional functions, e.g., the release of antimycotic hydroxybenzaldehydes, which are vital for stress compensation. Key words: elicitor-induced phenylpropanoids, cell wall reinforcement, hydroxycinnamoyl esters, lignin, caffeoyl-CoA-specific 3-O-methyltransferase, disease resistance response, parsley (Petroselinum crispum) cell cultures.

Characterization and Expression of Caffeoyl-Coenzyme A 3-O-Methyltransferase Proposed for the Induced Resistance Response of Vitis vinifera L

“…COMT activity was not induced to a significant extent under these conditions but increased steadily over the time of the experiments by a factor of 1.5 to 2.0 (Fig. 1B) strates (Matern et al, 1995;Meng and Campbell, 1996), and the corresponding activities were therefore measured in the crude grapevine extracts. Caffeate and 5-hydroxyferulate were methylated by COMT(s) at a constant ratio of approximately 1:3 (Fig.…”

“…Resveratrol and related phenolics started to accumulate after about 6 to 9 h under these conditions, and the yellow-white cells and the culture broth turned brown (data not shown). In contrast to many other plant cells (Tietjen et al, 1983;Graham and Graham, 1991) COMT and, in particular, CCoAOMT activities have been commonly considered as indicators of phenylpropanoid synthesis and lignification (Ye et al, 1994;Boudet et al, 1995;Matern et al, 1995). Low constitutive activities of both CCoAOMT and COMT were determined for the cultured grapevine cells (Fig.…”

“…The reinforcement triggered locally by pathogen invasion (Niemann et al, 1991) or fungal elicitation (Graham and Graham, 1991) causes drastic changes in the rigidity and digestibility of the cell wall and presents a major obstacle to the activities of lytic fungal enzymes (Nicholson and Hammerschmidt, 1992;Matern et al, 1995).…”

“…These results already point to a close link between SAR and the sensitization of phenylpropanoid metabolism, although the fact that the tissue phenotype in the SAR state was unchanged and required an additional fungal inoculation to release the enhanced lignification remains puzzling. The reinforcement with lignin-like materials requires the synthesis of feruloyl-and sinapoyl-CoAs (Walter, 1992;Boudet et al, 1995) and a nove1 route to these substrates was reported recently based on the sequential methoxylations of 4-coumarate:CoA ligase (Kneusel et al, 1989;Pakusch et al, 1989Matern et al, 1995). The methyltransferase involved, CCoAOMT, was cloned, and the expression of the enzyme activity appeared to be controlled by multiple parameters (Schmitt et al, 1991;Ye et al, 1994;Grimmig and Matern, 1997).…”

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

“…the space between the cell wall and the plasma membrane). Formation of these cell wall appositions (CWAs) or papillae is usually accompanied by a co-localised accumulation of phenolics and reactive oxygen species [2][3][4][5][6]. The complex process of sub-cellular cell wall remodelling is tightly linked to the rapid disassembly and subsequent focal reassembly of the plant cytoskeleton at fungal entry sites, which is indicative of a pathogen-triggered cell polarisation [6][7][8][9].…”