The highly buffered Arabidopsis immune signaling network conceals the functions of its components.
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 resilience by allowi...
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doaj-7f42e677e3f84ef0bea374a7663d55f62020-11-25T01:53:32ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042017-05-01135e100663910.1371/journal.pgen.1006639The highly buffered Arabidopsis immune signaling network conceals the functions of its components.Rachel A HillmerKenichi TsudaGhanasyam RallapalliShuta AsaiWilliam TrumanMatthew D PapkeHitoshi SakakibaraJonathan D G JonesChad L MyersFumiaki KatagiriPlant 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 resilience by allowing different parts of the network to compensate for loss of one another'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, in which 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-we call these sectors-in the flg22-responsive transcriptome. Many of these interactions result in network buffering. Resolved regulatory mechanisms 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 the regulatory mechanisms we resolved are not detectable by the traditional genetic approach of single-gene null-mutant analysis. Similar to potential pathogenic perturbations, null-mutant effects on immune signaling can be buffered by the network.http://europepmc.org/articles/PMC5417422?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Rachel A Hillmer Kenichi Tsuda Ghanasyam Rallapalli Shuta Asai William Truman Matthew D Papke Hitoshi Sakakibara Jonathan D G Jones Chad L Myers Fumiaki Katagiri |
spellingShingle |
Rachel A Hillmer Kenichi Tsuda Ghanasyam Rallapalli Shuta Asai William Truman Matthew D Papke Hitoshi Sakakibara Jonathan D G Jones Chad L Myers Fumiaki Katagiri The highly buffered Arabidopsis immune signaling network conceals the functions of its components. PLoS Genetics |
author_facet |
Rachel A Hillmer Kenichi Tsuda Ghanasyam Rallapalli Shuta Asai William Truman Matthew D Papke Hitoshi Sakakibara Jonathan D G Jones Chad L Myers Fumiaki Katagiri |
author_sort |
Rachel A Hillmer |
title |
The highly buffered Arabidopsis immune signaling network conceals the functions of its components. |
title_short |
The highly buffered Arabidopsis immune signaling network conceals the functions of its components. |
title_full |
The highly buffered Arabidopsis immune signaling network conceals the functions of its components. |
title_fullStr |
The highly buffered Arabidopsis immune signaling network conceals the functions of its components. |
title_full_unstemmed |
The highly buffered Arabidopsis immune signaling network conceals the functions of its components. |
title_sort |
highly buffered arabidopsis immune signaling network conceals the functions of its components. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS Genetics |
issn |
1553-7390 1553-7404 |
publishDate |
2017-05-01 |
description |
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 resilience by allowing different parts of the network to compensate for loss of one another'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, in which 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-we call these sectors-in the flg22-responsive transcriptome. Many of these interactions result in network buffering. Resolved regulatory mechanisms 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 the regulatory mechanisms we resolved are not detectable by the traditional genetic approach of single-gene null-mutant analysis. Similar to potential pathogenic perturbations, null-mutant effects on immune signaling can be buffered by the network. |
url |
http://europepmc.org/articles/PMC5417422?pdf=render |
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