Journal
FRONTIERS IN PLANT SCIENCE
Volume 4, Issue -, Pages -Publisher
FRONTIERS RESEARCH FOUNDATION
DOI: 10.3389/fpls.2013.00403
Keywords
resistance gene pair; temperature shift; EDS1 signaling; biotic stress; programed cell death; transcriptional reprograming
Categories
Funding
- Max-Planck Society
- Deutsche Forschungsgemeinschaft [SFB 670]
- BMBF-funded Plant-KBBE Trilateral BALANCE project
- IMPRS PhD fellowship
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In plant effector-triggered immunity (ETI), intracellular nucleotide binding-leucine rich repeat (NLR) receptors are activated by specific pathogen effectors. The Arabidopsis TIR (Toll-Interleukin-1 receptor domain)-NLR (denoted TNL) gene pair, RPS4 and RRS1, confers resistance to Pseudomonas syringae pv tomato (Pst) 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 Arabidopsis accession Ws-0, the RPS4(ws)/RRS1(ws) allelic pair governs resistance to Pst/AvrRps4 accompanied by host programed cell death (pcd). In accession Col-0, RPS4(col)/RRS1(col) effectively limits Pst/AvrRps4 growth without pcd. Constitutive expression of HA-Strepll tagged RPS4(col) On a 35S:RPS4-HS line) confers temperature-conditioned EDS/-dependent auto-immunity. Here we show that a high (28 degrees C, non-permissive) to moderate (19 degrees C, permissive) temperature shift of 35S:RPS4-HS plants can be used to follow defense-related transcriptional dynamics without a pathogen effector trigger. By comparing responses of 35S:RPS4-HS with 35S:RPS4-HS rrs 1-11 and 35S:RPS4-HS eds 1-2 mutants, we establish that RPS4(col) auto-immunity depends entirely on EDS1 and partially on RRS1(col). Examination of gene expression microarray data over 24 h after temperature shift reveals a mainly quantitative RRS1(col) contribution to up- or down-regulation of a small subset of RPS4(col)-reprogramed, EDS1-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(col) contributes to temperature-conditioned RPS4(col) auto-immunity and are consistent with activated RPS4(col) engaging RRS1(col) for resistance signaling.
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