Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/1/1997
Publication Date: N/A
Interpretive Summary: Plants respond to fungus diseases by producing substances that delay or stop fungal development at sites of infection. Plants do this by activating "defense" genes that control production of a variety of substances in the plant's cells around the point of attack. Some of the substances are known to be toxic to fungi. However, we do not know what most of the defense genes produce or how important they are in combating the attacking fungus. One way to gather evidence that a particular defense gene may be important in resistance is to study when it becomes activated in comparison with when the attacking fungus is blocked from developing in resistant plants. Genes that are activated before the fungus development is stopped may be essential for resistance to that disease. We studied defense genes in oats that are activated when the plants are attacked by the stem rust fungus. We found that several genes are activated in the first day or two after oat plants are inoculated with the rust fungus. These genes were activated shortly before we began to see evidence that the rust fungus had been stopped and was no longer developing in the infection sites. We also found that these genes were activated more strongly in plants with resistance to stem rust than in susceptible plants. This stronger activation may account for the difference in outcome of infection in resistant and susceptible plants. Focusing research on how these genes are activated will help scientists design oats and other crops with improved disease resistance.
Technical Abstract: Transcript accumulation patterns for six host response genes in oat inoculated with an incompatible isolate of Puccinia graminis f.sp. avenae (Pga-1H) were compared to patterns of hypersensitive cell death (HCD) and inhibition of colony elongation. HCD occurred at 4-6% of infection sites at 36 hr after inoculation (AI) increasing to only 26-32% of sites at 72 hr AI, whereas colony growth was completely or partially inhibited at 42-48 h AI. By 24-30 hr AI, transcripts of three genes accumulated preferentially in the incompatible or inappropriate interactions: 3 phosphoglycerate kinase (3-PGK), an enzyme of glycolysis, possibly associated with early respiratory increase; phenylalanine ammonia lyase (PAL), probably related to increased phenylpropanoid biosynthesis, and a gene of unknown function which hybridized to a cDNA, pCRL120, obtained from the incompatible interaction. By 36 hr AI, at the time HCD was beginning to occur, transcripts of a gene for glucose regulating protein 94(GRP94)began to accumulate. Finally, at 42-48 hr, in association with HCD and colony growth inhibition, transcripts of genes for a pathogenesis related protein (PR-1) and for thaumatin-like protein (tlp) accumulated. The results indicate a sequential series of gene activations, starting with 3-PGK, PAL and the gene corresponding to pCRL120, followed by GRP94, and ending with PR-1 and tlp.