Engineering Disease Resistance in Plants: An Overview Page: 250
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interactions, such defense-response genes are either not activated or are induced too late in the interaction
to prevent disease symptoms.6,7 These observations suggest that resistance could be engineered in plants
by (1) altering the timing and extent of induced defenses by constitutive expression of a natural induced
defense-response gene or by putting naturally occurring defense-response genes under the control of
stronger inducible promoters, or (2) by genetic manipulation of the dominant resistance genes per se.
The strategy of altering expression of defense-response genes could also include targeting expression
of novel antimicrobial proteins from foreign organisms, either constitutively or to the plant-pathogen
Some fungal and bacterial pathogens produce toxins which are responsible for the disease symptoms.8
In such cases, virulence is dominant and resistance is expressed through the ability of the host either
to not recognize the toxin (i.e., by lacking a toxin binding site) or to detoxify it. In such cases,
incorporation of toxin-insensitive binding sites or enzymes for detoxification may provide means of
Some fungal pathogens have acquired virulence by being able to detoxify the phytoalexins the host
produces as a part of its defensive arsenal.9 A basis of information now exists for engineering modified
phytoalexin structures which may be resistant to detoxification, or for transferring a phytoalexin biosyn-
thetic pathway from one plant to another which lacks that particular pathway. Such strategies will
generally necessitate the transfer of several genes; although this may pose complications, attempts in
this area should lead to further insights into the control of plant gene expression and the roles of
secondary metabolites in plants.
The following sections review the prospects for engineering fungal and bacterial resistance in plants
based on the above features of plant-pathogen interactions. For a more detailed background on the
molecular basis of resistance in plant-microbe interactions, the reader is referred to the reviews by
Lamb et al.,10 Dixon and Lamb," Dixon and Harrison,5 and Keen.'2 More details of engineered resistance
strategies can be found in the recent review by Lamb et al."
III. CHOICE OF PROMOTERS
A large number of plant defense-response genes have now been cloned.'4 Most of these are transcription-
ally activated in response to infection or exposure to microbial elicitor macromolecules.5 The promoters
of such genes could therefore be used to target expression of engineered transgenes encoding proteins
to enhance resistance. Before selecting a defense-response gene promoter for such studies, several
features of the promoter must be assessed. These include whether or not its expression is tissue or cell
type specific, whether it is affected by developmental or environmental cues other than infection, its
kinetics of activation in response to infection, and its extent of expression (i.e., promoter strength). If
the protective factor being introduced is not toxic to the plant, it may be best to use a promoter which
will deliver high-level constitutive expression; the cauliflower mosaic virus 35S promoter'5 or higher
expression derivatives with double enhancer elements'6 have been used successfully in a number of
cases. Indeed, the importance of the timing of defense gene activation in determining the outcome of
many plant-pathogen interactions suggests that having the newly engineered defensive barrier in place
prior to pathogen ingress should be beneficial. On the other hand, inducible promoters would be a
necessity if constitutive expression of the transgene or its ultimate product (e.g., phytoalexins) were
toxic to the plant or in any way compromised the ability of the plant to defend itself (e.g., by affecting
amino acid or energy metabolism in the case of very highly expressed proteins).
The properties of several plant defense-response gene promoters are outlined in Table 1. Many of
these show highly specific patterns of tissue and cell type expression. In some cases, it has proved
possible to separate cis-elements conditioning infection or elicitor inducibility from those determining
tissue-specific expression;" it may thus be possible to engineer a promoter which is only expressed in
response to pathogen attack.
To be of general use, a promoter must retain its potential for correct activation in species other than
that from which the gene was isolated. The examples in Table 1 indicate that most defense-response
gene promoters studied to date are active in heterologous species. Whether or not this is likely to be
universally true is not yet known, although it is interesting to note that the bean chs8 promoter, the
activation of which is a component of the induction of isoflavonoid phytoalexins in the host species,
is also induced by infection in tobacco,20 which does not use the flavonoid pathway for defense and
does not make isoflavonoids at all. Some monocot defense gene promoters are correctly expressed in
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Dixon, R. A.; Paiva, Nancy L. & Bhattacharyya, Madan Kumar. Engineering Disease Resistance in Plants: An Overview, chapter, 1995; [Boca Raton, Florida]. (https://digital.library.unt.edu/ark:/67531/metadc674022/m1/4/: accessed May 19, 2019), University of North Texas Libraries, Digital Library, https://digital.library.unt.edu; crediting UNT College of Arts and Sciences.