Interplay between MAMP‐triggered and SA‐mediated defense responses

Abstract

Summary: Plants respond to pathogen infection using an innate immune system with at least two distinct recognition mechanisms. One mechanism recognizes microbe‐associated molecular patterns (MAMPs). The other is based on resistance (R) genes and specifically recognizes certain pathogen virulence factors, including those delivered through the type III secretion system (TTSS) of bacteria. Salicylic acid (SA)‐mediated responses are an important part of the R gene‐mediated defense. Substantial overlaps between MAMP‐triggered and SA‐mediated responses have been reported. However, interactions between MAMP‐triggered and SA‐mediated signaling mechanisms have not been well documented. Here we report intimate interactions between MAMP‐triggered and SA‐mediated signaling. We found that SA accumulated at a higher level 6 h after treatment with a MAMP, flg22 or inoculation with Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) hrcC mutant, which is deficient in TTSS function. Disruptions of SA signaling components, such as SID2 and PAD4, strongly affected MAMP‐triggered responses monitored by expression profiling. We found two groups of genes that were induced by Pst DC3000 hrcC in an SA‐dependent manner. One group was SID2‐dependent at all time points, whereas the other was SID2‐independent at early time points and SID2‐dependent at later time points. Thus, the expression of the latter genes responds to MAMPs through both SA‐independent and SA‐dependent signaling mechanisms. Strong resistance to Pst DC3000 hrcC was dependent on SA signaling. These results indicate that the SA increase triggered by MAMPs is a major component of the MAMP‐triggered signaling mechanism, explaining the overlapping spectra of MAMP‐triggered and SA‐mediated responses.