Abstract
The heightening concern of consumers about the pesticide residues of food has resulted in the loss of or requirement for reregistration of some of the mainstay pesticides used in agriculture (Richardson 1989). As this process continues, the need for employing any and all natural processes that can contribute to plant protection becomes paramount. The abundance and low cost of foods to date has contributed to the low level of funding for plant research. The plant scientist is now facing an urgent demand for natural plant protection without an extensive backlog of supportive basic research. That is, we are expected to replace the rare, effective chemicals derived from millions of synthetically generated compounds with natural compounds (Bell 1981; Bailey and Mansfield 1982) that are painstakingly derived from natural defense responses in plants. Further, these compounds must also be effective when applied externally, be scrutinized for safety concerns, be reasonable in price, and be applicable to the existing agricultural practices.
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References
An, G., B. D. Watson, S. Stachel, M. P. Gordon, and E. W. Nester 1985. New cloning vehicles for transformation of higher plants. EMBO J. 42:277–284.
Bailey, J. A., and J. W. Mansfield. 1982. Phytoalexins. NY: Wiley.
Bell, A. A. 1981. Biochemical mechanisms of disease resistance. Ann. Rev. Plant Physiol. 32:21–81.
Bowles, D. J. 1990. Defense related proteins in higher plants. Ann. Rev. Biochem. 59:873–907.
Chiang, C. C., and L. A. Hadwiger. 1990. Cloning and characterization of a disease resistance response gene in pea induced by Fusarium solani. Mol. Plant MicrobeInteractions 3:75–87.
Daniels, C. H., B. W. Fristensky, W. Wagoner, and L. A. Hadwiger. 1986. Pea genes associated with non-host disease resistance to Fusarium are also active in race-specific disease resistance to Pseudomonas. Plant Mol. Biol. 8:309–316.
Dixon, R. A., and C. J. Lamb. 1990. Molecular communications in interactions between plants and microbial pathogens. Ann. Rev. Plant Physiol. 41:339–367.
Fernandez, M. R., and M. C. Heath. 1989. Interaction of the non-host French bean plant (Phaseolus vulgaris) with parasitic and saprophytic fungi. I. Fungal development on and in killed, untreated, heat-treated, or Blasticidin S treated leaves. Can. J. Bot. 67:661–669.
Flor, H. H. 1971. Present status of the gene for gene concept. Ann. Rev. Phytopathol. 9:275–296.
Fristensky, B., D. Horovitz, and L. A. Hadwiger. 1988. cDNA sequences for pea disease resistance response genes. Plant Mol. Biol. 11:713–715.
Fristensky, B., R. C. Riggleman, W. Wagoner, and L. A. Hadwiger. 1985. Gene expression in susceptible and disease resistant interactions of peas induced with Fusarium solani pathogens and chitosan. Physiol. Plant Pathol. 27:15–28.
Hadwiger, L. A. 1988. Possible role of nuclear structure in disease resistance in plants. Phytopathology 78:1009–1014.
Hadwiger, L. A., and J. M. Beckman. 1980. Chitosan as a component of pea-Fusarium solani interactions. Plant Physiol. 66:205–211.
Hadwiger, L. A., and W. Wagoner. 1983a. Effect of heat shock on the mRNA-directed disease resistance response of peas. Plant Physiol. 72:553–556.
Hadwiger, L. A., and W. Wagoner. 1983b. Electrophoretic patterns of pea and Fusarium solani proteins synthesized in vitro which characterize the compatible and incompatible interactions. Physiol. Plant Pathol. 23:153–162.
Hadwiger, L. A., C. C. Chiang, and D. Horovitz. 1991. Expression of disease resistance response genes in near isogenic pea cultivars following challenge by Fusarium solani race 1. Physiol. Molec. Plant Pathol. (in press).
Heath, M. C. 1987. Host vs. non-host resistance. In Molecular Strategies for Crop Protection, ed. C. J. Arntzen and C. Ryan, pp. 25–34. New York: Liss.
Keen, N. T. 1990. Gene-for-gene complimentarity in plant-pathogen interactions. Ann. Rev. Genet. 24:447–463.
Kendra, D. F., and L. A. Hadwiger. 1984. Characterization of the smallest chitosan oligomer that is maximally antifungal to Fusarium solani and elicits pisatin formation in Pisum sativum. Exp. Mycol. 8:276–281.
Kendra, D. F., D. A. Christian, and L. A. Hadwiger. 1989. Chitosan oligomers from Fusarium solani/pea interactions, chitinase/β-glucanase digestion and fungal wall chitin actively inhibit fungal growth and induce disease resistance. Physiol. Mol. Plant Pathol. 35:215–230.
Klee, H., R. Horsch, and S. Rogers. 1987. Agrobacterium-medicated plant transformation and its further applications to plant biology. Ann. Rev. Plant Physiol. 38:467–486.
Kuc, J., and C. Preisig. 1984. Fungal regulation of disease resistance mechanisms in plants. Mycologia 76:767–784.
LeGuay, J. J., M. Piecoup, J. Puckett, and J. P. Jouanneau. 1988. Common responses of cultured soybean cells to 2,4-D starvation and fungal elicitor treatment. Plant Cell Rep. 7:19–22.
Lindgren, P. B., N. J. Panopoulos, B. J. Staskawicz, and D. Dahlbeck. 1988. Genes required for pathogenicity and hypersensitivity are conserved and interchangeable among pathovars of Pseudomonas syringae. Mol. Gen. Genet. 211:499–506.
Matton, D. P., and N. Brisson. 1989. Cloning, expression, and sequence conservation of pathogenesis-related gene transcripts of potato. Mol. Plant Microbe Interactions 2:325–331.
Mauch, F., L. A. Hadwiger, and T. Boiler. 1984. Ethylene: Symptom, not signal for the induction of chitinase and β-1,3-glucanase in pea pods by pathogens and elicitors. Plant Physiol. 76:607–611.
Mauch, F. C., L. A. Hadwiger, and T. Boller. 1988. Purification and characterization of two β-1,3-glucanase differentially regulated during development and in response to fungal infection. Plant Physiol. 87:325–333.
Newport, J. W., and D. J. Forbes. 1987. The nucleus: Structure, function and dynamics. Ann. Rev. Biochem. 56:535–566.
Richardson, L. 1989. Registration reality. Agriculture Age 33:13–15.
Riggleman, R. C., B. Fristensky, and L. A. Hadwiger. 1985. The disease resistance response in pea is associated with increased levels of specific mRNAs. Plant Mol. Biol. 48:81–86.
Schmidt, R. J., F. A. Burr, M. J. Aukerman, and B. Burr. 1990. Maize regulatory gene opaque-2 encodes a protein with a leucine-zipper motif that binds to zein DNA. Proc. Natl. Acad. Sci. (USA) 87:46:50.
Silver, P. A. 1991. How proteins enter the nucleus. Cell 64:489–497.
Singh, K., E. S. Dennis, J. G. Ellis, D. J. Llewellyn, J. G. Tokuhisa, J. A. Wahleithner, and W. J. Peacock. 1990. OCSBF-1 a maize Ocs enhancer binding factor: Isolation an expression during development. Plant Cell 2:891–903.
Teasdale, J., D. Daniels, W. C. Davis, R. Eddy Jr., and L. A. Hadwiger. 1974. Physiological and cytological similarities between disease resistance and cellular incompatibility responses. Plant Physiol. 54:690–695.
Wagoner, W., D. C. Loschke, and L. A. Hadwiger. 1982. Two-dimensional electrophoresis analysis of in vivo and in vitro synthesis of proteins in peas inoculated with compatible and incompatible Fusarium solani. Physiol. Plant Pathol. 20:99–107.
Wessler, S., and S. Hake. 1990. Maize harvest. Plant Cell 2:495–499.
Yarwood, C. E. 1973. Some principles of plant pathology, II. Phytopathology 63:1324–1325.
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Hadwiger, L.A. (1992). Toward the Genetic Engineering of Disease Resistance in Plants: The Transfer of Pea Genes to Potatoes. In: Bhatnagar, D., Cleveland, T.E. (eds) Molecular Approaches to Improving Food Quality and Safety. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-8070-2_5
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DOI: https://doi.org/10.1007/978-1-4684-8070-2_5
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