Plants respond to infection by accumulating low-molecular-weight antimicrobial stress metabolites called phytoalexins. The phytoalexins are generally lipophilic substances that are products of a plant's secondary metabolism, and they often accumulate at infection sites to concentrations which are inhibitory to the development of fungi and bacteria. Resistance and susceptibility in plants are not determined by the presence or absence of genetic information for resistance mechanisms, including biosynthetic pathways for phytoalexin synthesis, but, rather, by the speed with which the information is expressed, the activity of the gene products, and the magnitude of the resistance response. Unlike the antibody-antigen component of the immune system in animals, low specificity is the general rule for the induction of phytoalexin accumulation and their activity against microorganisms. Annual plants can be systemically immunized against diseases caused by fungi, bacteria, and viruses by restricted infection with the pathogens, avirulent forms of pathogens, or compounds formed in immunized plants. Immunization induces plants to respond rapidly to infection with a multicomponent resistant response. The biosynthesis and accumulation of phytoalexins is one component of this resistant response. Resistance may be elicited by components in the walls and cell surfaces of fungi and bacteria and by compounds liberated from cells, their walls, or surfaces. Resistance can be enhanced or suppressed by products produced by the pathogen, the host, or by their interaction. The successful pathogen avoids recognition by the plant as nonself, suppresses the resistance response, or detoxifies its products. The actors in this play for survival on the metabolic level include the shikimate, acetate-malonate, and acetate-mevalonate pathways; glucans; oligogalacturonates; glycoproteins; lipopolysaccharides; and polyunsaturated fatty acids. The play is directed by the genetic information of host and pathogen, and this direction is at the level of recognition and not by the presence or absence of mechanisms to contain the development of infectious agents.
|Number of pages||18|
|Journal||Archives of Biochemistry and Biophysics|
|State||Published - Feb 1 1985|
Bibliographical noteFunding Information:
The authors’ work reported in this paper was supported in part by Grants ‘78-59-2211-O-1063 and 7B30-O-185 from the United States Department of Agriculture, and grants from the R. J. Reynolds Corporation, the Rockefeller Foundation, and Graduate School of the University of Kentucky. Journal Paper Number 84-11-50 of the Kentucky Agricultural Experiment Station, Lexington, Kentucky.
ASJC Scopus subject areas
- Molecular Biology