Submitted to: American Phytopathological Society
Publication Type: Literature Review
Publication Acceptance Date: July 30, 2008
Publication Date: January 1, 2012
Citation: Bell, R.L. 2012. Biotechnological approaches to enhance fire blight resistance. In: T. van der Zwet, N. Orolaza-Halbrendt, and W. Zeller, editors. Fire blight – history biology, and management. St. Paul, MN. American Phytopathological Society. p. 212-226. Technical Abstract: Fire blight, caused by the bacterium Erwinia amylovora, is the most serious disease of apples, pears, and quince, most major fruit and rootstock cultivars being susceptible. Modern plant biotechnologies provide methods of enhancing the resistance to fire blight in apples and pears of existing scion and rootstock cultivars. The earliest research focused on genes encoding natural antimicrobial lytic peptides and synthetic derivatives, but increasing use has been made of genes of bacterial or plant origin directly involved in pathogenicity or host response, respectively. Somaclonal variants are clones which differ from the original source genotype due to genetic or epigenetic changes that are more or less stable and heritable, but polyploidization may have been a factor in enhanced resistance of regenerant pear clones. A similar range of lesion lengths was observed in artificially inoculated apple clones transformed with a synthetic antimicrobial cecropin gene and clones transformed with only the vector, but transgenic approaches have, in general, resulted in some significant improvement over untransformed clones and have received more research attention. The improvement of fire blight resistance through a transgenic approach has been achieved in several apple and pear scion cultivars and in apple rootstocks. There is considerable variation among clones in the degree of reduction of symptoms, but several genes have resulted in at least a 50 percent reduction in symptoms, with a small number as high as 95 percent. The lytic peptide genes used include: attacin E and cecropin B, components of the hemolymph immune system of the silk moth, synthetic cecropin derivatives. Genes which inhibit Erwinia amylovora pathogenicity factors include those producing mammalian lactoferrin, an iron-chelating glycoprotein, to interfere with an iron-binding sideophore which enhances pathogen growth and survival under the low-iron conditions of host tissues,and extracellular polysaccharide-depolymerases that degrade polysaccharides enveloping bacterial cells. Overexpression of the pathogen harpin Nea protein, a secreted component of the type III secretory pathway required for pathogenicity, appears capable of promoting induction of host resistance responses. Gene silencing of host cell wall proteins which interact with the pathogenicity factor DspE is another approach. Overexpressioin of the MpNPR1 gene, a key to initiating a cascade of host disease response genes, has enhanced resistance, and other host genes are being identified. Genetic mapping has identified several markers linked to quantitative trait loci (QTLs) controlling variation in resistance in apple and pear, and which may prove to be a useful tool for breeding new resistant cultivars.