AJ Cann
Pseudomonas syringae is a widespread bacterial pathogen that causes disease on a broad range of economically important plant species. In order to infect, P. syringae produces a number of toxins and uses a type III secretion system to deliver effector proteins into eukaryotic cells. This mechanism is essential for successful infection by both plant- and animal-associated bacteria as bacterial mutants are no longer pathogenic. However, the molecular function and host targets of the vast majority of effectors remain largely unknown.
Plant immunity relies on a complex network of small-molecule hormone signaling pathways (see: Wasternack, C. (2007) Jasmonates: an update on biosynthesis, signal transduction and action in plant stress response, growth and development. Annals of botany, 100(4), 681-697). Classically, salicylic acid (SA) signaling mediates resistance against biotrophic and hemi-biotrophic microbes such as P. syringae, whereas a combination of jasmonic acid (JA) and ethylene (ET) pathways activates resistance against necrotrophs such as the fungus Botrytis cinerea. SA and JA/ET defense pathways generally antagonize each other – elevated resistance against biotrophs is often correlated with increased susceptibility to necrotrophs and vice versa. The collective contribution of these two hormones during plant-pathogen interactions is crucial to the success of the interaction. Remarkably, some Pseudomonas strains have evolved a sophisticated strategy for manipulating hormonal balance by producing the toxin coronatine (COR), which mimics the plant hormone jasmonate-isoleucine (JA-Ile). The JA-Ile pathway plays a key role in plant immunity by activating defenses against fungal pathogens, while promoting bacterial growth by inhibiting the salicylic acid (SA)-dependent defenses required for Pseudomonas resistance.
A recent paper in PLOS Biology reports that the effector HopX1 from a Pseudomonas syringae strain that does not produce COR exploits an alternative evolutionary strategy to activate the JA-Ile pathway. HopX1 encodes a cysteine protease that interacts with and promotes the degradation of key JA pathway repressors, the JAZ proteins. Correspondingly, ectopically expressing HopX1 in the model plant Arabidopsis induces the expression of JA-dependent genes, and natural infection with Pseudomonas producing HopX1 promotes bacterial growth in a similar fashion to COR. These results highlight a novel example by which a bacterial effector directly manipulates core regulators of hormone signaling to facilitate infection:
Eurekalert
Alun Salt
botanyone
