Poster
Frank LW Takken
Associate Professor
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Thomas R. Aalders
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Fleur Gawehns
dr
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Hanna Richter
dr
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Annemarie Vermeulen
Msc
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Harrold A. Van Den Burg
Prof. Dr.
University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Fusarium oxysporum (Fo) causes Fusarium wilt disease in many crops. The fungus manipulates its hosts using SIX effectors. The broadly conserved effector SIX8 targets specific members of the Topless (TPL) family (Aalders et al., 2024). TPLs are transcriptional co-repressors and SIX8-targeted tomato TPL1 and TPL2 proteins are important for susceptibility. A tpl1;tpl2 double mutant exhibits near complete Fusarium resistance. Likewise, Arabidopsis tpr1;tpl double mutants show near complete Fo resistance. To elucidate SIX8 function it was produced in Arabidopsis Col-0. Six8 transformants exhibited a temperature-dependent growth phenotype, constitutive PR1 and PR2 expression, and local cell death, all indicative for constitutive immune signalling. TPR1 interacts with SNC1, a temperature sensitive NLR-type immune receptor (Zhu et al. 2010 PNAS) To test involvement of TPL, TPR1, SNC1 and SNC1-signalling components (i.e. eds1, pad4, and NahG) Arabidopsis mutants were transformed with SIX8. The SIX8 phenotype fully reverted in TPL, TPR1, SNC1 and EDS1knockouts and partially in NahG plants.These data indicate that SNC1 guards TPL and TPR1 and monitors their perturbation by SIX8. Identification of SNC1 as guard of Topless proteins sustains their involvement in resistance and susceptibility. A possible mechanism of how SIX8 triggers SNC1-mediated immunity and manipulates TPLs will be presented, providing new leads to reduce susceptibility to Fo.