Extracellular vesicle signatures and protein citrullination are modified in shore crabs () infected with sp.

Epizootiologists recurrently encounter symbionts and pathobionts in the haemolymph (blood equivalent) of shellfish. One such group is the dinoflagellate genus , which contains several species that cause debilitating disease in decapod crustaceans. The shore crab acts as a mobile reservoir of microparasites, including sp., thereby posing a risk to other co-located commercially important species, e.g. velvet crabs (). Despite the widespread prevalence and documented seasonality of infection dynamics, there is a knowledge gap regarding host-pathogen antibiosis, namely, how avoids the host's immune defences. Herein, we interrogated the haemolymph of -positive and -negative crabs for extracellular vesicle (EV) profiles (a proxy for cellular communication), alongside proteomic signatures for post-translational citrullination/deimination performed by arginine deiminases, which can infer a pathologic state. Circulating EV numbers in parasitized crab haemolymph were reduced significantly, accompanied by smaller EV modal size profiles (albeit non-significantly) when compared to -negative controls. Differences were observed for citrullinated/deiminated target proteins in the haemolymph between the parasitized and control crabs, with fewer hits identified overall in the former. Three deiminated proteins specific to parasitized crab haemolymph were actin, Down syndrome cell adhesion molecule (DSCAM), and nitric oxide synthase - factors that contribute to innate immunity. We report, for the first time, sp. could interfere with EV biogenesis, and that protein deimination is a putative mechanism of immune-modulation in crustacean- interactions.