Turtlegrass (Thalassia testudinum) undergoes a coordinated hypersensitive response when challenged with pathogenic Labyrinthula sp.

Infection of the marine subtropical seagrass Thalassia testudinum Banks ex König by pathogenic Labyrinthula sp. was found to induce lesion progression, alterations to the host's oxidative metabolism, and production of defense metabolites over the early stages of infection (monitored over a 72-hr time course). By 48-hr post-infection, host oxygen consumption, internal reactive oxygen concentrations, and caspase-3 proteolytic activity reached their highest levels. The formation of reactive oxygen species (ROS) and nitric oxide (NO) were detected in T. testudinum lesions by use of redox-sensitive probes/substrates and fluorescent imaging. To our knowledge, this work represents the first time NO has been detected in a marine angiosperm within the context of plant-pathogen interactions. Hydrogen peroxide production and lesion expansion were highly regulated in the presence of diphenyleneiodonium, catalase, and c-PTIO, suggesting crosstalk between ROS and NO activity. Using a nontargeted metabolomics approach, succinic acid, 3-phenylpropionic acid, and methyl p-coumarate concentrations were found to significantly increase following Labyrinthula infection. The generation of characteristic seagrass wasting disease lesions likely results from cell death via the host's hypersensitive response (HR) as well as direct degradation of tissue by the pathogen. These results highlight the existence of a co-evolutionary arms race between seagrasses and Labyrinthula that shape the ecology and evolution of seagrass wasting disease.