Salads Under Siege, Episode 7: Decoys and traps


In this episode, I will describe (molecular) innovations that some plant species have adopted during host-pathogen Co-evolution. To do so, reading my previous posts (see below) would help form a bigger picture of how all of this works on both mechanistic and evolutionary levels.

Figure 1. Decoys and traps. Plants have evolved mechanisms akin to mousetraps to trap and kill of their foes (pathogens). Such mechanisms are described below. Source. *DISCLAIMER: I do not own this or any other mousetraps (2 cats not included).

I already went into detail about how pathogens can suppress plant immunity. Pathogens can secrete proteins or other compounds that have the specific goal to interact and disable a process on its host. This can be the action of an enzyme that works against the microbe, factors that drive secretion of antimicrobials, enzymes that are involved in immune signalling (kinases or ubiquitin ligases for example) as well as factors that drive transcription (gene expression) in plants. 

I also described how plants might counteract such pathogen-derived hardware (weapons) and turn the interaction on its head. Besides modification of the effector target (using random mutation and subsequent selection), I explained how plants also deploy receptors that detect the presence of the effector or its modification and trigger immunity. How do plants achieve recognition of effectors and how can they be so specific?

Here, I will describe some of the latest discoveries that represent clever new ways in which hosts can trick their pathogens. More specifically, I will explain the concept of host target decoys and integrated decoy mechanism found in plants. These mechanisms explain to some degree how plants can detect specific effectors without carrying millions of receptors to do the job.

A little background on WRKY transcription factors, regulators of immunity

It is well established that plants employ specific transcription factors to induce the expression of genes upon microbial invasion. One such class is called the WRKY transcription factor class (These proteins feature a WRKY sequence motif at the N-terminus along with other domains and act as transcription factors) and some proteins within this family, play roles in immune responses. As you may imagine, if a protein is very important in host defense, it makes sense for a pathogen to target such a factor to prevent the onset of defensive gene expression. Indeed, as it turns out, effectors have been identified that can target WRKY proteins (Leroux et al., 2015; Sarris et al., 2015). In fact, many bacterial pathogens have independently evolved effector molecules, able to perturb WRKY function which normally, upon pathogen perception, binds to host chromatin and initiates defense gene expression. These observations convincingly show how important these transcription factors must be for immunity in plants and therefore, how critical it must be for these microbes to inhibit their function.

Figure 2. Helicopters discharging decoys. Flares produce heat which will fool heat-seaking missiles. In essence, they are decoys. Source. Note: It is ironic that I love investigating the war between host and pathogens. I am averse to war (conducted by humans) and this figure is not meant to celebrate or lend support to war in any way. In fact, I have justified the use of this image as it shows a defensive capability rather then an aggressive attack style image).

OK, back to decoys. How can plants protect against this wide variety of microbes, each of which is after ruining their precious defensive capabilities? The answer is 'decoy.' Sometimes, genes get duplicated or to put it in another way, get copied and land elsewhere in the plant genome where they either degenerate, retain their function (identical to its original twin sister or evolve to take on a new role. In the case of decoys, these gene doubling events led to neo-functionalization in which one copy of the gene mutated such that its encoded protein still looks like a target but not have a role in resistance anymore. Rather, these mimics have evolved to bind effectors with higher affinity, catching these proteins before they can damage the host immune system (van der Hoorn and Kamoun, 2008).

Figure 3. The Buff-tip Moth (Phalera bucephala). A good example of mimicry in nature. A moth looking like the tip of a broken Branch! This trick is analogous to molecular mimicry where protein domains appear to have a genuine cellular function but actually are dedicated effector traps Source

Where does that leave integrated decoys? Remember the receptor proteins that I mentioned earlier? You know, the host proteins that can recognize pathogen effectors and initiate these massive defense responses? It turns out that some members of this large protein family, carry domains that strongly resemble host proteins that are targeted by pathogen effectors.

An example you say? Let's go back to the WRKY transcription factors that drive immunity in plants! Previous work established that some effectors from bacterial pathogens can modify their target through acetylation of key transcription factors. The pathogen Ralstonia solanacearum effector PopP2 can modify and inactivate WRKY transcription factors by acetylating a key lysine residue in the WRKY motif (Leroux et al., 2015; Sarris et al., 2015).

Figure 4. Evidence showing that a pathogen effector (PopP2) acetylates a large group of WRKY transcription factors. Purification of WRKY transcription factors after co-expression with either PopP2 or negative controls, allows detection of acetylation of target proteins using an Lys-actetylation specific antibody (4th row from the top; Modified from Leroux et al., 2015; Figure 4). 

Now critically, the examination of the RRS1 protein sequence (a receptor) identified a small domain that resembled WRKY transcription factors (Figure 5). It was also shown that this domain can be acetylated in the same way as WRKY transcription factors, suggesting that RRS1 contains a WRKY decoy domain. Indeed, functional and proteomic analyses helped establish that the WRKY motif in the decoy domain is in fact acetylated.

Figure 5. Schematic representation of RRS1-R, a receptor protein with an integrated decoy that mimics WRKY transcription factors. A lysine (K) residue within the conserved WRKY motif is targeted and N-acetylated by effector PopP2, which activates a signalling complex to condition immunity. Modified from Leroux et al., 2015; Figure 1).

Thus RRS1 is a chimeric receptor protein that uses its integrated decoy domain to trick the pathogen effector. The effector binds the mimic and modifies it in the same way as it would with the real target. Modification of the decoy domain, however, leads to structural changes in the entire receptor which in turn, acts as the signal alerting the host on the presence of the pathogen. This signal is transmitted and amplified throughout the host cell to initiate a fast and robust response.

Figure 6. Evidence that RRS1-R containing the WRKY motif is acetylated by PopP2. RRS1-R was expressed in plants in combination with PopP2 and negative controls, purified (IP) and probed with antibodies that recognise acetylated lysine residues (4th row from the top). Modified from Figure 1 found in Leroux et al., 2015.

What are the implications?

This work has shown that the immense co-evolutionary pressures have selected for pretty smart tricks that plants use to gain an advantage (my next post will describe a similar trick in pathogens). Evolution has told us that WRKY transcription factors are important targets. Genome sequence analyses have identified other receptors, carrying integrated decoys derived from other host protein domains, that immediately tell us which functions are critical to the plant. It also explains how plants only need a limited set of receptors to detect pathogen effectors. They can simply do so by "guarding" those proteins that are critical for immunity. This saves plants the hassle of carrying a receptor for every single pathogen effector. 


Le Roux, C., Huet, G., Jauneau, A., Camborde, L., Trémousaygue, D., Kraut, A., ... & Raffaele, S. (2015). A receptor pair with an integrated decoy converts pathogen disabling of transcription factors to immunity. Cell, 161(5), 1074-1088.

Sarris, P. F., Duxbury, Z., Huh, S. U., Ma, Y., Segonzac, C., Sklenar, J., ... & Wirthmueller, L. (2015). A plant immune receptor detects pathogen effectors that target WRKY transcription factors. Cell, 161(5), 1089-1100.

van der Hoorn, R. A., & Kamoun, S. (2008). From guard to decoy: a new model for perception of plant pathogen effectors. The Plant Cell, 20(8), 2009-2017.

To read more about our salads and their adversaries, please find links to other episodes below:

What sets a pathogen apart from its innocent relatives?

Episode 1

Episode 2

Episode 3

Episode 4

Episode 5

Episode 6

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