The Fusarium oxysporum effector Six8 manipulates plant immunity through association with the transcriptional co-repressors TPL and TPR1
F. TAKKEN (1), F. Gawehns (2), M. de Sain (2), P. Houterman (2), H. Dekker (3), D. Valkenburg (2), H. van den Burg (2), M. Rep (2), G. van den Ackervecken (4), H. Richter (2) (1) University of Amsterdam - Mol. Plant Pathology, Netherlands; (2) University of Amsterdam - Mol. Plant Pathology, Netherlands; (3) University of Amsterdam - mass spectrometry, Netherlands; (4) Utrecht University - Plant-Microbe Interactions,, Netherlands

Fusarium oxysporum f. sp. lycopersici (Fol) is the causal agent of tomato wilt disease. During infection the fungus secretes at least 40 proteins - including 30 enzymes and 14 candidate effectors - into the xylem sap. For the Six8 effector we found a potential host target; pull-down assays identified a member of the TOPLESS (TPL) family. The interaction of SIX8 with TPL and with a TPL homolog (TPR1-Topless Related 1) was confirmed in Y2H and BifC experiments. Silencing TPL/TPR1 in tomato resulted in increased resistance to Fol, classifying TPLs as as genuine susceptibility genes. TPLs are co-repressors interacting with transcription factors that are involved in development, hormone signaling, and in “SNC1-mediated” defense mechanisms1. SNC1 is a NB-LRR resistance protein, providing a direct link between Six8 and host defense signaling. Transgenic Arabidopsis plants expressing SIX8 exhibit a temperature-dependent dwarf phenotype and show constitutive defense gene (PR1 and PR2) expression, suggesting a direct link to SNC1-mediated defenses. Arabidopsis T-DNA insertion lines lacking SNC1 or components of the SNC1- defense pathway (i.e. tpl, tpr1, tpr3, eds1, pad4, and NahG) have been transformed with SIX8 to identify the pathways affected by Six8. Bioassays on SIX8-containing Arabidopsis plants using P. syringae and H. parasitica revealed that NB-LRR resistance proteins other than SNC1 are unaffected. This study identifies TPL as a genuine Six8 effector target. A possible mechanism of how Six8 triggers SNC1-mediated immune signaling will be presented, providing new leads to use effector-targets for disease resistance. 

Abstract Number: P17-622
Session Type: Poster