Effector / 14-3-3 complexes

Impact of effector/14-3-3 complex formation during infection:

Collaborative project with Prof. Guido Sessa and Laboratory, Department of Molecular Biology and Ecology of Plants, Tel Aviv University, Israel

Mounting evidence indicates that multiple 14-3-3 isoforms are required for proper execution of plant immune responses during infection (Oh and Martin, 2011; Oh et al., 2010; Taylor et al., 2012; Yang et al., 2009) and that specific T3SEs physically associate with a subset set of these 14-3-3s to subvert and/or co-opt 14-3-3 function to promote pathogenicity (Giska et al., 2013; Li et al., 2013; Taylor et al., 2012; Teper et al., 2013). We thus hypothesize that bacterial pathogens may have evolved a core suite of T3SEs to manipulate 14-3-3 function at distinct nodes in host immune signaling during infection. In recent collaborative work with Dr. Guido Sessa at Tel Aviv University, we have recently performed comprehensive genetic and biochemical studies using the Xe-tomato pathosystem to elucidate the role of eleven tomato 14-3-3 isoforms (i.e. TFTs) in PTI and effector-triggered immunity (ETI), and to identify the suite of Xe T3SEs that form effector/TFT complexes in planta. Our initial work on the characterization of the XopQ/TFT4 interaction was recently published (Teper et al., 2013).

Notably, two important conceptual outcomes emerged from our collaboration this year: 1) All TFTs isoforms contribute at some level to anti-Xe immunity in tomato. This was unexpected as we anticipated that only a subset of the isoforms might contribute to plant disease resistance (i.e. PTI and/or ETI). Our work thus suggests that TFTs are resident components of immune complexes, whereby they serve specific and likely redundant roles. The identity of such complexes is poorly understood. Our efforts to develop molecular tools and transgenic plant lines to study specific TFT isoforms will enable us and others to identify and characterize specific TFT-containing immune complexes. 2) A small group of Xe effectors interact with various TFT isoforms. These findings indicate a subset of Xe T3SEs have evolved to recruit and/or target TFTs to promote pathogenesis during infection. Intriguing preliminary data suggests that one or more of these T3SEs may promote destabilization of specific TFT isoforms in planta. Future work is aimed to biochemically characterize Xe T3SE-TFT complexes in planta to determine the mechanisms by which this suite of Xe T3SEs subvert TFT function.