Abstract
Our previous experiments showed that infection of tobacco (Nicotiana tabacum) plants with Tobacco mosaic virus (TMV) leads to an increase in homologous recombination frequency (HRF). The progeny of infected plants also had an increased rate of rearrangements in resistance gene-like loci. Here, we report that tobacco plants infected with TMV exhibited an increase in HRF in two consecutive generations. Analysis of global genome methylation showed the hypermethylated genome in both generations of plants, whereas analysis of methylation via 5-methyl cytosine antibodies demonstrated both hypomethylation and hypermethylation. Analysis of the response of the progeny of infected plants to TMV, Pseudomonas syringae, or Phytophthora nicotianae revealed a significant delay in symptom development. Infection of these plants with TMV or P. syringae showed higher levels of induction of PATHOGENESIS-RELATED GENE1 gene expression and higher levels of callose deposition. Our experiments suggest that viral infection triggers specific changes in progeny that promote higher levels of HRF at the transgene and higher resistance to stress as compared with the progeny of unstressed plants. However, data reported in these studies do not establish evidence of a link between recombination frequency and stress resistance.
Highlights
Our previous experiments showed that infection of tobacco (Nicotiana tabacum) plants with Tobacco mosaic virus (TMV) leads to an increase in homologous recombination frequency (HRF)
How do plants that lack a resistance gene respond to infection? We have previously reported that the compatible interaction between Tobacco mosaic virus (TMV) and tobacco (Nicotiana tabacum ‘SR1’) plants lacking the TMV resistance N gene results in the production of a systemic signal
We have previously shown that infection of these transgenic tobacco plants with TMV increased HRF in infected leaves as well as in distant noninfected tissues (Kovalchuk et al, 2003a)
Summary
Our previous experiments showed that infection of tobacco (Nicotiana tabacum) plants with Tobacco mosaic virus (TMV) leads to an increase in homologous recombination frequency (HRF). The latter one depends on direct or indirect recognition of pathogen avirulence gene products by plant resistance gene products (Whitham et al, 1994; Durrant and Dong, 2004) Pathogen recognition during this incompatible interaction triggers complex events, including a local hypersensitive response that manifests itself as a booster of radical production and activation of the salicylic aciddependent pathway and necrotic lesions, which working together restrict pathogen spread.
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