Abstract

The lipid transfer protein (LTP) DEFECTIVE IN INDUCED RESISTANCE1 (DIR1) is a key mobile component of the systemic acquired resistance (SAR) response. Recent evidence suggests that a DIR1-like paralog occasionally compensates for the loss of DIR1 in the dir1-1 Ws-2 mutant. Here, we demonstrate that a dir1-2 mutant in the Col-0 background is SAR-defective, while DIR1-like knockdowns are SAR-competent. Moreover, protein-protein interaction assays demonstrate that DIR1 interacts with DIR1-like and other LTPs. Further investigation of these LTPs suggests a role for LTP2 in SAR. Our results highlight the importance of multiple lipid transfer proteins for SAR in Arabidopsis.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call