| Literature DB >> 28811287 |
Noriyuki Hatsugai1, Daisuke Igarashi1,2, Keisuke Mase1, You Lu1, Yayoi Tsuda1, Suma Chakravarthy3, Hai-Lei Wei3, Joseph W Foley4,5, Alan Collmer3, Jane Glazebrook1, Fumiaki Katagiri6.
Abstract
Since signaling machineries for two modes of plant-induced immunity, pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), extensively overlap, PTI and ETI signaling likely interact. In an Arabidopsis quadruple mutant, in which four major sectors of the signaling network, jasmonate, ethylene, PAD4, and salicylate, are disabled, the hypersensitive response (HR) typical of ETI is abolished when the Pseudomonas syringae effector AvrRpt2 is bacterially delivered but is intact when AvrRpt2 is directly expressed in planta These observations led us to discovery of a network-buffered signaling mechanism that mediates HR signaling and is strongly inhibited by PTI signaling. We named this mechanism the ETI-Mediating and PTI-Inhibited Sector (EMPIS). The signaling kinetics of EMPIS explain apparently different plant genetic requirements for ETI triggered by different effectors without postulating different signaling machineries. The properties of EMPIS suggest that information about efficacy of the early immune response is fed back to the immune signaling network, modulating its activity and limiting the fitness cost of unnecessary immune responses.Entities:
Keywords: deep perturbation; fitness cost of immunity; network resilience; plant immune signaling network
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Year: 2017 PMID: 28811287 PMCID: PMC5599791 DOI: 10.15252/embj.201796529
Source DB: PubMed Journal: EMBO J ISSN: 0261-4189 Impact factor: 11.598