AUTHOR=Heidrich Katharina , Tsuda Kenichi , Blanvillain-Baufumé Servane , Wirthmueller Lennart , Bautor Jaqueline , Parker Jane E.

TITLE=Arabidopsis TNL-WRKY domain receptor RRS1 contributes to temperature-conditioned RPS4 auto-immunity

JOURNAL=Frontiers in Plant Science

VOLUME=4

YEAR=2013

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2013.00403

DOI=10.3389/fpls.2013.00403

ISSN=1664-462X

ABSTRACT=<p>In plant effector-triggered immunity (ETI), intracellular nucleotide binding-leucine rich repeat (NLR) receptors are activated by specific pathogen effectors. The <italic>Arabidopsis</italic><italic>TIR</italic> (<italic>Toll-Interleukin-1 receptor domain</italic>)-<italic>NLR</italic> (denoted <italic>TNL</italic>) gene pair, <italic>RPS4</italic> and <italic>RRS1</italic>, confers resistance to <italic>Pseudomonas syringae</italic> pv <italic>tomato</italic> (<italic>Pst</italic>) strain DC3000 expressing the Type III-secreted effector, AvrRps4. Nuclear accumulation of AvrRps4, RPS4, and the TNL resistance regulator EDS1 is necessary for ETI. RRS1 possesses a C-terminal “WRKY” transcription factor DNA binding domain suggesting that important RPS4/RRS1 recognition and/or resistance signaling events occur at the nuclear chromatin. In <italic>Arabidopsis</italic> accession Ws-0, the <italic>RPS4<sup>Ws</sup></italic>/<italic>RRS1<sup>Ws</sup></italic> allelic pair governs resistance to <italic>Pst</italic>/AvrRps4 accompanied by host programed cell death (pcd). In accession Col-0, <italic>RPS4<sup>Col</sup></italic>/<italic>RRS1<sup>Col</sup></italic> effectively limits <italic>Pst</italic>/AvrRps4 growth without pcd. Constitutive expression of HA-StrepII tagged <italic>RPS4<sup>Col</sup></italic> (in a <italic>35S:RPS4-HS</italic> line) confers temperature-conditioned <italic>EDS1</italic>-dependent auto-immunity. Here we show that a high (28°C, non-permissive) to moderate (19°C, permissive) temperature shift of <italic>35S:RPS4-HS</italic> plants can be used to follow defense-related transcriptional dynamics without a pathogen effector trigger. By comparing responses of <italic>35S:RPS4-HS</italic> with <italic>35S:RPS4-HS</italic><italic>rrs1-11</italic> and <italic>35S:RPS4-HS</italic><italic>eds1-2</italic> mutants, we establish that <italic>RPS4<sup>Col</sup></italic> auto-immunity depends entirely on <italic>EDS1</italic> and partially on <italic>RRS1<sup>Col</sup></italic>. Examination of gene expression microarray data over 24 h after temperature shift reveals a mainly quantitative <italic>RRS1<sup>Col</sup></italic> contribution to up- or down-regulation of a small subset of <italic>RPS4<sup>Col</sup></italic>-reprogramed, <italic>EDS1</italic>-dependent genes. We find significant over-representation of WRKY transcription factor binding W-box cis-elements within the promoters of these genes. Our data show that RRS1<sup>Col</sup> contributes to temperature-conditioned RPS4<sup>Col</sup> auto-immunity and are consistent with activated RPS4<sup>Col</sup> engaging RRS1<sup>Col</sup> for resistance signaling.</p>