A Plant Gene Up-Regulated at Rust Infection Sites

Abstract

Expression of the fis1 gene from flax (Linum usitatissimum) is induced by a compatible rust (Melampsora lini) infection. Infection of transgenic plants containing a ␤-glucuronidase (GUS) reporter gene under the control of the fis1 promoter showed that induction is highly localized to those leaf mesophyll cells within and immediately surrounding rust infection sites. The level of induction reflects the extent of fungal growth. In a strong resistance reaction, such as the hypersensitive fleck mediated by the L6 resistance gene, there is very little fungal growth and a microscopic level of GUS expression. Partially resistant flax leaves show levels of GUS expression that were intermediate to the level observed in the fully susceptible infection. Sequence and deletion analysis using both transient Agrobacterium tumefaciens expression and stable transformation assays have shown that the rust-inducible fis1 promoter is contained within a 580-bp fragment. Homologs of fis1 were identified in expressed sequence tag databases of a range of plant species including dicots, monocots, and a gymnosperm. Homologous genes isolated from maize (Zea mays; mis1), barley (Hordeum vulgare; bis1), wheat (Triticum aestivum; wis1), and Arabidopsis encode proteins that are highly similar (76%-82%) to the FIS1 protein. The Arabidopsis homologue has been reported to encode a ⌬ 1 -pyrroline-5-carboxylate dehydrogenase that is involved in the catabolism of proline to glutamate. RNA-blot analysis showed that mis1 in maize and the bis1 homolog in barley are both up-regulated by a compatible infection with the corresponding species-specific rust. The rust-induced genes homologous to fis1 are present in many plants. The promoters of these genes have potential roles for the engineering of synthetic rust resistance genes by targeting transgene expression to the sites of rust infection.For successful parasitism of plants by fungal pathogens, particularly in the case of obligate, biotrophic phytopathogens such as rust fungi, it is apparent that the pathogen has evolved strategies for manipulating host cellular metabolism, morphology, and development (Clancy and Coffey, 1980; Sutton and Shaw, 1982, 1986; Scholes, 1992; Roy, 1993; Chou et al., 2000; Hall and Williams, 2000). Successful infection of the host plant by the pathogen requires the induction of a subset of pathogen genes that are essential for pathogenicity (Pieterse et al., 1993; Talbot et al., 1993; Rogers et al., 1994; Hwang et al., 1995; Hahn and Mengden, 1997; Hahn et al., 1997). Less clear is the role and expression of specific host genes that may be required for successful pathogen infection of the plant. Identification of host genes induced during a successful pathogen infection may provide insight into the compatible host/pathogen interaction at a molecular level.The fis1 gene of flax (Linum usitatissimum) was identified as a host gene up-regulated during a successful or compatible flax rust (Melampsora lini) infection (Roberts and Pryor, 1995). RNA-blot analysis of fis1 demonstr...

Engineering disease resistance in plants

“…However, extensive testing of the flax Fis1 promoter fused to the UidA gene showed also activation, although much less in incompatible rust-flax interactions (Ayliffe et al, 2002). This finding stresses the importance of carefully testing promoter-reporter gene fusions under various conditions.…”

“…Homologues of this Fis1 gene have been detected in barley, maize, wheat and Arabidopsis, and rust responsiveness has been confirmed in barley and maize (Ayliffe et al, 2002).…”

The Melampsora lini AvrL567 Avirulence Genes Are Expressed in Haustoria and Their Products Are Recognized inside Plant Cells

“…One of the primary functions of haustoria seems to be to facilitate nutrient uptake from the host (Hahn and Mendgen, 2001). Haustoria formation also induces structural changes in the host cell, including cytoskeletal rearrangements, nuclear migration, and chromatin condensation (Kobayashi et al, 1994;Heath, 1997), and there is some evidence that compatible rusts can suppress host defense responses and influence host cell metabolism (Mellersh and Heath, 2001;Ayliffe et al, 2002;Voegele and Mendgen, 2003). However, the signals leading to these changes are not known.…”

Proline Metabolism and Its Implications for Plant-Environment Interaction

“…Cell death (apoptosis) activated by proline metabolism and P5C has also been described in mammalian systems. Another report showed induction of P5CDH by compatible fungal infection (Ayliffe et al, 2002), possibly a mechanism used by the pathogen to keep P5C levels low and inhibit cell death and the hypersensitive response. Although the possible role of P5C as an inducer of programmed cell death has been mentioned in a number of places, there is no information on the underlying mechanism except that the salicylic acid pathway may be involved (Deuschle et al, 2004).…”