Open AccessActivation of the Promoter of the Tnt1 Retrotransposon in Tomato After Inoculation with the Fungal Pathogen Cladosporium fulvum
Author(s) -
Corinne Mhiri,
P.J.G.M. de Wit,
Marie–Angèle Grandbastien
Publication year - 1999
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi.1999.12.7.592
Subject(s) - pathosystem , biology , cladosporium , retrotransposon , gene , genetics , hypersensitive response , gene expression , nicotiana tabacum , botany , microbiology and biotechnology , plant disease resistance , mutant , aspergillus , transposable element
The copia-like Tnt1 element of tobacco is one of the few active plant retrotransposons and is transcriptionally activated, in tobacco and in heterologous species, by biotic and abiotic stress factors. In order to establish more precisely the link between Tnt1 activation and plant defense responses, the expression of the Tnt1 promoter was studied in a gene-for-gene pathosystem, the interaction between tomato and the fungal pathogen Cladosporium fulvum. In compatible interactions, Tnt1 expression is highly induced throughout the leaf regions colonized by the fungus, while in incompatible interactions Tnt1 induction is transient and localized in distinct foci. Tnt1 expression after fungal inoculation parallels the differential activation of tomato defense genes. Tnt1 expression is induced by nonspecific factors of plant or fungal origin present in apoplastic fluids of leaf tissues infected by virulent races of C. fulvum, but is also activated by specific factors resulting from the interaction between fungal avirulence peptides and plant resistance genes. Tnt1 activation by apoplastic fluids containing avirulence peptides of C. fulvum is detected soon after elicitation. These results demonstrate that Tnt1 transcriptional activation correlates with biological responses of tomato to infection by C. fulvum and is mediated through signals originating from both race-specific and non-race-specific perception pathways.