Of PAMPs and effectors: the blurred PTI-ETI dichotomy

Abstract

Typically, pathogen-associated molecular patterns (PAMPs) are considered to be conserved throughout classes of microbes and to contribute to general microbial fitness, whereas effectors are species, race, or strain specific and contribute to pathogen virulence. Both types of molecule can trigger plant immunity, designated PAMP-triggered and effector-triggered immunity (PTI and ETI, respectively). However, not all microbial defense activators conform to the common distinction between PAMPs and effectors. For example, some effectors display wide distribution, while some PAMPs are rather narrowly conserved or contribute to pathogen virulence. As effectors may elicit defense responses and PAMPs may be required for virulence, single components cannot exclusively be referred to by one of the two terms. Therefore, we put forward that the distinction between PAMPs and effectors, between PAMP receptors and resistance proteins, and, therefore, also between PTI and ETI, cannot strictly be maintained. Rather, as illustrated by examples provided here, there is a continuum between PTI and ETI. We argue that plant resistance is determined by immune receptors that recognize appropriate ligands to activate defense, the amplitude of which is likely determined by the level required for effective immunity.

Figure 1.

A Variation on the Zigzag Model to Describe the Evolution of Chitin Signaling in the Interaction between C. fulvum and Tomato. The C. fulvum PAMP chitin activates PTI in tomato plants, presumably upon perception by the tomato homolog of the rice cell surface receptor CEBiP. Thus far, a chitin-triggered HR has not been observed in tomato. To overcome PTI, C. fulvum employs the abundantly secreted LysM effector Ecp6 that binds chitin, thereby preventing activation of Sl-CEBiP. Since LysM effectors are widely conserved in the fungal kingdom, they qualify as PAMPs, and Ecp6-mediated PTI suppression therefore should be referred to as PAMP-triggered susceptibility (PTS). Tomato genotypes that have evolved to recognize Ecp6 develop an HR upon Ecp6 infiltration and presumably carry a cell surface receptor for this molecule, tentatively called C. fulvum resistance to Ecp6 (Cf-Ecp6), again resulting in PTI (PTI2). The question mark indicates that subsequent susceptibility can again be provoked by C. fulvum, either through mutation of the Ecp6 protein such that it still sequesters chitin fragments but is no longer recognized by Cf-Ecp6 or by producing an effector that suppresses Sl-CEBiP signaling in an alternative manner. (Adapted by permission from Macmillan Publishers Ltd.: Nature; Jones and Dangl [2006].)