In my previous posts (see below for a full list), I have listed some of the reasons why the study of proteins or molecules (medicine) that wreak havoc in host cells is of interest. For this post, I left out one other important reason. One impetus, for us to study particular effector molecules, is that evolution has demonstrated that this pathogen-encoded weaponry is crucial in the host-pathogen running game!
What do we mean by this? If a secreted protein is critical for infection by a pathogen, one can expect a plant host to try to target it or use it to its advantage in some way. Genome sequencing, functional and biochemical studies have demonstrated that precisely! Critically, plants have acquired and evolved vast repertoires of intracellular receptors, specialized in the detection of pathogen effector molecules. Perception of these effectors by these receptors raises the alarm and shuts the proverbial candy shop.
By saying "to shut down the candy shop," I put things rather mildly. A better analogy, often used in the plant biology field is to say that plants execute a scorched earth tactic. In this tactic, the plant deliberately kills cells in which pathogen effectors are detected, creating a highly unpleasant environment in which many pathogens cannot thrive. The response associated with this response is called the hypersensitive response (HR) and is widely known to be a form of programmed cell death (Coll et al., 2011). Yes, you read this right! The HR is determined by the genes encoding the receptors in the plant and a series of genetically encoded regulators that make sure the HR response is robust enough on the one hand but does not spread to healthy (non-infected) tissues (Coll et al., 2011; Lorrain et al., 2003).
Fig. 1 Image of a plant leaf displaying symptoms of a hypersensitive response upon recognition of a pathogen effector. The burned appearance is due to programmed cell death, activated upon the perception of an effector or its activity by an intracellular receptor. Source
Importantly and besides these genetic factors in the host plant, the effector coding genes in the pathogen that prevent infection when expressed, form another genetic requirement for plant cell death. This phenomenon, in which virulence (infection) or avirulence (resistance) is determined by factors present in both host and pathogen, is also called the gene-for-gene hypothesis and was first proposed by Harold Flor. Importantly, this elegant model seems to apply to many, if not most, pathosystems (Flor 1971).
While this may seem counterintuitive (why would a pathogen carry genes that are to its detriment), from a running game's perspective, it makes sense. In nature, plants are diverse with some members of a species carrying one set of receptors (perhaps capable of recognizing a particular pathogen strain), while others may not harbour the appropriate receptor. If there are enough susceptible plants around, the pathogen will survive and bare the cost of being defeated every once in a while.
Maintaining such an avirulence factor is especially worthwhile if its loss results in a fitness penalty. As long as the number of susceptible plants in the population is sufficient, and the avirulence factor is important for fitness, it will be maintained in the pathogen population. Displacement may occur, however, when new virulent strains arrive that do not require the avirulence gene. In other words, pathogens that have come up with a new solution to the "fitness penalty problem".
To cap this post off, I hope you now appreciate that plants do not sit by idly, waiting for pathogens to destroy their tissues. Over time and collectively (as a population) they are generating new receptor varieties, able to detect effector from pathogens. It is those receptors that can recognize key effectors, which will make an impact on plant health. In my next post, I will look at the running game in a more evolutionary and population biology perspective. Watch this space!
To read more about our salads and their adversaries, please find links to other episodes below:
Coll, N. S., Epple, P., & Dangl, J. L. (2011). Programmed cell death in the plant immune system. Cell death and differentiation, 18(8), 1247.
Flor, H. H. (1971). Current status of the gene-for-gene concept. Annual review of phytopathology, 9(1), 275-296.
Lorrain, S., Vailleau, F., Balagué, C., & Roby, D. (2003). Lesion mimic mutants: keys for deciphering cell death and defense pathways in plants?. Trends in plant science, 8(6), 263-271.