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The Arabidopsis thaliana transcriptome in response to Agrobacterium tumefaciens. | LitMetric

AI Article Synopsis

  • Agrobacterium tumefaciens, a unique plant pathogen, introduces T-DNA into plant genomes but lacks typical hrp genes found in other bacterial pathogens.
  • Researchers used a microarray to study the gene response of Arabidopsis plants infected with Agrobacterium, identifying distinct gene sets that were either induced or suppressed 48 hours post-infection.
  • The induced genes are linked to plant defense, while the repressed genes, which are associated with cell proliferation, suggest a regulatory mechanism involving specific upstream elements, shedding light on plant-pathogen signaling pathways.

Article Abstract

The pathogen Agrobacterium tumefaciens infects a broad range of plants, introducing the T-DNA into their genome. Contrary to all known bacterial phytopathogens, A. tumefaciens lacks the hypersensitive response-inducing hrp genes, although it introduces numerous proteins into the plant cell through a type IV secretion system. To understand the timing and extent of the plant transcriptional response to this unusual pathogen, we used an Arabidopsis 26,000-gene oligonucleotide microarray. We inoculated Arabidopsis cell cultures with an oncogenic Agrobacterium strain and analyzed four biological replicates to identify two robust sets of regulated genes, one induced and the other suppressed. In both cases, the response was distinct at 48 h after infection, but not at 24 h or earlier. The induced set includes genes encoding known defense proteins, and the repressed set is enriched with genes characteristic of cell proliferation even though a growth arrest was not visible in the inoculated cultures. The analysis of the repressed genes revealed that the conserved upstream regulatory elements Frankiebox (also known as "site II") and Telobox are associated with the suppression of gene expression. The regulated gene sets should be useful in dissecting the signaling pathways in this plant-pathogen interaction.

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Source
http://dx.doi.org/10.1094/MPMI-19-0665DOI Listing

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