Combined roles of ethylene and endogenous peptides in regulating plant immunity and growth.

The gaseous hormone ethylene (ET) controls diverse aspects of plant life (1). In innate immunity, ET is often associated with resistance to necrotrophic pathogens (2). ET also plays a role in induced systemic resistance that is triggered by the perception of beneficial microbes in the rhizosphere (2). ET is often antagonistic with the hormones salicylic acid and jasmonic acid (2). However, perception of pathogen-associated molecular patterns (PAMPs) by plant pattern-recognition receptors (PRRs) leads to the production of ET, salicylic acid, and jasmonic acid, and all three hormones are required for local PAMPinduced resistance to pathogens (3, 4). The precise role of ET in PAMP-triggered immunity (PTI) was therefore unclear. In PNAS, Tintor et al. and Liu et al. (5, 6) present convincing evidence for a role of ET in an amplification loop required for sustained PTI, and some growth responses triggered by the hormone. The best-studied PRRs are the Arabidopsis leucine-rich repeat receptor kinases (LRRRKs) FLS2 and EFR that perceive bacterial flagellin (or flg22) and EF-Tu (or elf18), respectively (7). Following ligand-binding, FLS2 and EFR recruit the regulatory LRR-RK BAK1 leading to transphosphorylation events between these proteins, as well as with the cytoplasmic kinase BIK1 (7–9). Previous genetic analyses revealed that ET perception and signaling are required for proper FLS2 expression (10, 11). Indeed, the ET-activated transcription factors EIN3 and EIL1 bind the FLS2 promoter to regulate FLS2 transcription (10). This finding suggests that flg22-induced ET production enables amplification and maintenance of PTI by replenishment of FLS2 at the plasma membrane, which is otherwise degraded following flg22 perception (12). In a forward genetic screen for elf18-insensitive mutants, Tintor et al. (5) identified a unique allele of the ERlocalized protein EIN2, which is the central regulator of ET signaling (13). Notably, although they could confirm that EIN2 is required for proper FLS2 expression, no effect on the transcript accumulation of EFR could be observed in ein2 mutants, suggesting that ET could play an additional role. Specifically, the authors found that ET signaling is important for a subset of elf18-induced responses, such as the burst of reactive oxygen species (ROS), transcriptional reprogramming, callose deposition, but not MAP kinase activation. The key question that then arose was: how does ET regulate these responses? A first hint was provided by the observation that PROPEP2 is among the elf18induced genes that are regulated in an EIN2and EIN3/EIL1-dependent manner (5). PROPEP2 is part of a seven-member family of propeptides that are proposed to act as damage-associated molecular patterns (14). PROPEP gene expression is regulated by diverse stimuli, and derived synthetic Pep peptides induce immune responses similar to those triggered by PAMPs (3, 15–19). Perception of Pep peptides depends on the related LRR-RKs PEPR1 and PEPR2 that show sequence and functional homologies with FLS2 and EFR (16, 20). Although PROPEP genes have been proposed to be part of an amplification loop for PTI, this hypothesis has never been tested directly. Tintor et al. (5) hypothesize that the expression of PROPEP2 and subsequent potential recognition by PEPR1/2 may contribute to certain responses triggered by elf18. Consistently, the elf18induced expression of PR-1 (a late immune marker gene) was strongly reduced in the double-mutant pepr1 pepr2. Importantly, pepr1 pepr2 plants were also more susceptible to spray-infection with the hemibiotrophic bacterium Pseudomonas syringae pv. tomato (Pto) DC3000 and affected in the elf18-induced resistance to this bacterium. The second hint came with the study from Liu et al. (6), which provides more mecha-