Putative sugar-binding proteins additively promote systemic acquired resistance in parallel with salicylic acid
C. VLOT (1), E. Pabst (1), H. Breitenbach (1), M. Wenig (1), C. Knappe (1) (1) Helmholtz Zentrum Muenchen, Institute of Biochemical Plant Pathology, Germany

Systemic acquired resistance (SAR) is a broad-spectrum salicylic acid (SA)-dependent disease resistance in the systemic healthy tissues of locally infected plants. SAR is associated with a number of putative long distance signals, including the non-protein amino acid pipecolic acid (PIP), the C9 lipid-derived compound azelaic acid (AzA), and glycerol-3-phosphate (G3P) that appear to act mostly in parallel with SA. Similarly, the putative sugar-binding LEGUME LECTIN-LIKE PROTEIN1 (LLP1) promotes SAR in parallel with SA. Here, we will present recent data suggesting that LLP1 acts in SAR together with PIP and G3P, but not necessarily with AzA (currently preliminary), and will propose an SA-independent pathway that is essential for SAR. In that pathway, LLP1 is supported by LECTIN1 (LEC1) and/or LEC2 that share ~70% nucleotide sequence homology with LLP1 and ~97% with each other. A lec1 single knock out mutant was SAR-deficient. Moreover, a SAR trigger in plants undergoing RNAi-mediated silencing of LLP1, LEC1, and LEC2 enhanced the systemic susceptibility of the plants to a Pseudomonas syringae cSystemic acquired resistance (SAR) is a broad-spectrum salicylic acid (SA)-dependent disease resistance in the systemic healthy tissues of locally infected plants. SAR is associated with a number hallenge infection. Petiole exudate experiments further showed that LLP1, LEC1, and/or LEC2 are essential for SAR in the systemic, SAR signal perceiving tissue. Together, the data suggest that LLP1, LEC1, and/or LEC2 act additively in SA-independent SAR signal recognition or propagation in the systemic tissue, possibly in association with PIP and G3P.


Abstract Number: C15-1
Session Type: Concurrent