Abstract
Active defense of plants against fungal or bacterial pathogens often involves the rapid death of cells in intimate contact with the invading microorganism. Accompanying this so-called hypersensitive response (HR) are rapid localized changes in host metabolism which lead to the synthesis of potential defensive barriers; these include the accumulation of low Mr antimicrobial compounds termed phytoalexins, the deposition of phenolic material and hydroxyproline-rich glycoproteins (HRGPs) in the host cell wall, and the synthesis of hydrolytic enzymes. The exact relationship between the HR and phytoalexin accumulation is still somewhat vague; in some systems, hypersensitive cell death appears to be a pre-requisite for induction and accumulation of phytoalexins in neighboring healthy cells (Bailey 1982), whereas phytoalexin synthesis can be initiated in suspension cultured cells in the absence of serious effects on cell viability (Hamdan and Dixon 1986). It is, however, well documented that molecules from plant pathogenic fungi have the ability to induce both hypersensitive-type cell necrosis and/or phytoalexin accumulation in plant cells. These so-called elicitors often originate from the fungal cell wall.
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Dixon, R.A. et al. (1990). Elicitors and Defense Gene Activation in Cultured Cells. In: Ranjeva, R., Boudet, A.M. (eds) Signal Perception and Transduction in Higher Plants. NATO ASI Series, vol 47. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83974-0_22
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DOI: https://doi.org/10.1007/978-3-642-83974-0_22
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