Meeting the Challenge of Yellow Rust in Cereal Crops - ICARDA

for the biosynthesis of a large number of products derived from the
phenylpropane skeleton (He-Ping, Fischer and Liao, 2001). Phenylpropanoid
synthesis is activated as a response to stress, which includes elicitor treatment,
pathogen infection, wounding and UV irradiation. Since changes in PAL
activity are key events controlling the synthesis of phenylpropanoids, PAL has
become one of the most extensively studied enzymes in plants. Infection of
wheat leaves with the stem rust fungus or injection with an elicitor from this
fungus causes the accumulation of lignin or lignin-like polymers (lignification).
The specific inhibition of lignification by enzyme inhibitors increases disease
susceptibility to stem rust fungus in wheat. He-Ping, Fischer and Liao (2001)
reported that in the Sr6 near-isogenic line in the background of cv. Prelude, the
transcription of the mRNA from PAL gene (Wpalt1) are initiated quickly (4–8
days after infection) in copious quantity, but in susceptible cv. Prelude,
without Sr6, the PAL gene is transcripted too late and in small quantities.
Moreover, it has been shown that Wpalt1 expression was high in roots and
moderate in stem, but with no detectable expression found in leaves. It
indicates that PAL production is tissue specific. Therefore, it supports the idea
that some required factors for defence against pathogens are induced by
infection through signal transduction and transferred from other tissues to the
defending cells.
Role of plant disease resistance genes
Considerable knowledge has now been accumulated on the biochemical and
genetic bases of disease resistance, while the use of resistant cultivars has
become a valuable strategy to control crop disease. Within only the past few
years, disease resistance genes against distinct pathogen types have been
isolated. Intriguingly, the proteins encoded by resistance genes from different
species against different pathogens have many features in common
(Hammond-Kosack and Jones, 1997).
In race- and cultivar-specific disease resistance, rapid activation of the
defence response is mediated by a specific recognition event, involving the
product of an Avr gene in the pathogen and the corresponding resistance (R)
gene in the plant (Flor, l971). Many plant-pathogen interactions are of this
type. R genes are presumed to enable plants to detect the product(s) of the Avr
gene of the pathogen, and to initiate signal transduction to activate defence.
Isolation of resistance genes has revealed five main classes of sequences of
production to activate a range of defence mechanisms. Discovery of the
structure of the R gene provides insight into R gene function and evolution,
and should lead to novel strategies for disease control (Hammond-Kosack and
Jones, 1997). In the last few years, many R genes have been isolated that confer
resistance to pathogens, including viruses, bacteria, fungi and nematodes.
Several lines of evidence convincingly indicate that a kinase signalling
cascade may originate from the specific recognition of the products of the plant
R gene and corresponding pathogen Avr gene (Sessa and Martin, 2000).
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