Temporal accumulation patterns of defence response gene transcripts in relation to resistant reactions in oat inoculated with Puccinia graminis

K. C. Lin, W. R. Bushnell, A. G. Smith, L. J. Szabo

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24 Scopus citations

Abstract

Transcript accumulation patterns for six defence response genes in oat inoculated with an incompatible isolate of Puccinia graminis f.sp. avenae (Pga-1H) or an isolate of an inappropriate forma specialis, P. graminis f.sp. tritici (Pgt-8D), were compared to the occurrence of hypersensitive cell death (HCD) and inhibition of colony elongation. HCD here occurred at 4-6% of infection sites by 36 h after inoculation (AI) increasing to only 26-32% of sites at 72 h AI, whereas colony growth was completely or partially inhibited at 42-48 h AI, indicating that HCD was not a major factor in growth inhibition. By 24-30 h 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), related to increased phenylpropanoid biosynthesis, and a gene of unknown function which hybridized to a cDNA, pCRL120, previously obtained from the incompatible interaction. These transcripts accumulated before HCD or fungal growth inhibition, implicating activation of the three genes in early events leading to resistance. By 36 h AI, at the time HCD was beginning to occur, transcripts of a gene for the glucose-regulating protein 94 (GR P94) began to accumulate in response to isolate Pga-1H. Finally, at 42-48 h, 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 sequential activation of genes, beginning with 3-PGK, PAL and the gene corresponding to pCRL120, followed by GR P94, and ending with PR-1 and tlp.

Original languageEnglish (US)
Pages (from-to)95-114
Number of pages20
JournalPhysiological and Molecular Plant Pathology
Volume52
Issue number2
DOIs
StatePublished - Feb 1998

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