Mystery solved: How the atypical pair Mi-1.2 and SERK1 regulate aphid resistance?
I. KALOSHIAN (1), H. Peng (1), S. Mantelin (2), G. Hicks (2), F. Takken (3) (1) University of California Riverside, U.S.A.; (2) University of California Riverside, U.S.A.; (3) University of Amsterdam, Netherlands

Somatic embryogenesis receptor kinases (SERKs) are transmembrane receptors involved in plant immunity. Tomato carries three SERK members. One of these, SERK1, is required for Mi-1.2-mediated resistance to potato aphids (PA; Macrosiphum euphorbiae). Mi-1.2 encodes a CC-NLR that besides PAs confers resistance to additional phloem-feeding insects and to root-knot nematodes. How SERK1 participates in Mi-1.2-mediated resistance is unknown and no Mi-1.2 cognate pest effectors have been identified. We studied the mechanistic involvement of SERK1 in Mi-1.2-mediated resistance. We showed that PA saliva and PA protein extracts induce the Mi-1.2 defense marker WRKY72b, indicating that both saliva and extracts contain a Mi-1.2 recognized effector. Resistant tomato Motelle (Mi-1.2/Mi-1.2) plants overexpressing SERK1 were found to display enhanced resistance to PAs. Confocal microscopy revealed that Mi-1.2 localizes at three distinct subcellular compartments, namely the plasma membrane, cytoplasm and the nucleus. Coimmunoprecipitation experiments in these tomato plants, and in Nicotiana benthamiana transiently expressing Mi-1.2 and SERK1, showed that Mi-1.2 and SERK1, and not the other two SERKs, co-localize in a microsomal complex. Interestingly, BiFC analysis showed that the interaction of Mi-1.2 and SERK1 distinctively changes in the presence of PA saliva suggesting a model in which a constitutive complex at the plasma membrane participates in defense signalling upon effector binding.

Abstract Number: C24-5, P17-652
Session Type: Concurrent