The Mechanisms Of AtPTR3 Resistance Against Botrytis Cinerea

Plants in the natural environment suffer a lot of biotic stresses from pathogens such as bacteria,fungi,virus,oomycetes and the pathogens may cause serious damage.In order to defense against the pathogen infection,plants acquired a complicated immune system.At PTR3(Arabidoposis thaliana Peptide Transporter 3),belongs to PTR protein family,is induced by SA,Me JA and wounding and required for the resistance against Botrytis cinerea.In this study,At PTR3(Hereinafter referred to as PTR3)-interacting proteins were identified to figure out the molecular mechanisms of PTR3.The results are as follows:At first,disease assays showed that two PTR3 T-DNA insertion mutants,ptr3-5 and ptr3-4,were susceptibile to B.cinerea.Furthermore,we demonstrated that PTR3 interacted with BAK1 on plasmamembrane in vivo by Bi FC and PTR3 interacted with the LRR domain of BAK1.And the interaction of PTR3 with itself required BAK1.We had screened6 × Myc-PTR3/ptr3-5 and 6 × Myc-PTR3/bak1-4 transgenetic lines for the study of phosphorylation sites of PTR3.The following Bi FC screening found that Pro PEP1 and Pro PEP3 interacted with PTR3 and the phosphorylation sites of PTR3,S367,S376 and T380 were essential for the interaction between PTR3 and Pro PEP1.We had got PTR3 and Pro PEP1 co-transgenic lines for Co-IP and PTR3(3A)/ptr3-5 and PTR3(3D)/ptr3-5transgenic lines for inoculation experiment.