Time course transcriptional profiles of the Arabidopsis thaliana response to flg22 infiltration for all combinatorial genotypes of the alleles dde2-2, ein2-1, pad4-1, and sid2-2.
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ABSTRACT: Plant immunity protects plants from numerous potentially pathogenic microbes. The biological network that controls plant inducible immunity must function effectively even when network components are targeted and disabled by pathogen effectors. Network buffering could confer this robustness by allowing different parts of the network to compensate for loss of each other’s functions. Networks rich in buffering rely on interactions within the network, but these mechanisms are difficult to study by simple genetic means. Through a network reconstitution strategy, where we disassemble and stepwise reassemble the plant immune network that mediates Pattern-Triggered-Immunity, we have resolved systems-level regulatory mechanisms underlying the Arabidopsis transcriptome response to the immune stimulant flagellin-22 (flg22). These mechanisms show widespread evidence of interactions among major sub-networks—the components that we call sectors—in the flg22-responsive transcriptome. Many of these interactions result in network buffering. Resolved regulatory mechanisms also show unexpected patterns for how the jasmonate (JA), ethylene (ET), phytoalexin-deficient 4 (PAD4), and salicylate (SA) signaling sectors control the transcriptional response to flg22. We demonstrate that many of these mechanisms are hidden from the traditional genetic approach of single-gene null-mutant analysis. As potential pathogenic perturbations to the network, null-mutant effects can be buffered by the immune network as well.
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE78735 | GEO | 2017/03/01
SECONDARY ACCESSION(S): PRJNA313379
REPOSITORIES: GEO
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