Scleractinian corals (phylum Cnidaria, class Anthozoa) have innate immunological responses against infections. Research has recently suggested that corals also possess an adaptivelike immunological repertoire that recognizes specific pathogens and allografts. While evolutionarily distinct, the corals' innate and adaptive-like immunity systems are not mutually exclusive because the phagocytic cells of the non-specific, innate immune system may activate specific adaptive immunological responses. Warming oceans may immunocompromise coral hosts, making them more susceptible to tropical marine diseases, independent of the virulence of the pathogen. The ability of corals to ward off both primary and opportunistic infections, through adaptive-like mechanisms, may play a critical role in the corals' ability to fight future disease infection. Here we show evidence that corals possess immunological repertoires that extend well beyond simple innate defenses. The extent to which corals have developed such an adaptive-like immune repertoire will determine whether corals will survive climate change and other anthropogenic disturbances.KEY WORDS: Coral · Anthozoan genome · Coral immunology · Holobiont · Coral amoebocytes · Symbionts · Compromised-host hypothesis · Acropora millepora Resale or republication not permitted without written consent of the publisherDis Aquat Org 90: [85][86][87][88][89][90][91][92] 2010 brates contain only innate-immune defenses. The Hildemann group found that isografts (using the same colony) of the Hawaiian stony coral Montipora verrucosa were consistently compatible and fused within days of grafting, whereas allografts (from different colonies) resulted in soft-tissue death. Furthermore, the reaction time was accelerated by almost 50% when the same allograft pairs were reset. The authors summarized their results as showing 'both specificity in transplantation alloimmunity and extensive antigenic polymorphism among genetically separate M. verrucosa. ' (Hildemann et al. 1977). Moreover, researchers discovered that Vibrio shiloi, the bacteria that previously infected the stony coral Oculina patagonica in the eastern Mediterranean, is now lysed upon entering the coral tissue . How is such an expanded immunological repertoire possible for scleractinian corals?Metazoan invertebrates have evolved polymorphic histocompatibility mechanisms without the use of antibodies. For example, the innate-immune response of a freshwater hydrozoan polyp was found to be mediated by unconventional toll-like receptor (TLR) signaling (Bosch et al. 2009). Additionally, genetic studies of a marine hydrozoan, Hydractinia symbiolongicarpus, revealed an invertebrate histocompatibility complex. Tools are now at hand to isolate homologs of higher chordate immune system molecules and identify invertebrate allorecognition determinants (Mokady & Buss 1996, Cadavid et al. 2004, Dishaw & Litman 2009). This type of genetic approach has not yet been fully applied to reef corals.Conventional wisdom suggests that scleractini...

Parasites have been increasingly recognized as participants in indirect ecological interactions, including those mediated by parasite-induced changes to host behaviour (trait-mediated indirect interactions or TMIIs). In most documented examples, host behaviours altered by parasites increase susceptibility to predation because the predator is also a host (host-manipulation). Here, we test for a TMII in which a parasitic copepod modifies the predator-prey interaction between a small goby host and several larger predatory fish. Gobies compete for crevices in the reef to avoid predation and goby mortality increases more rapidly with increasing refuge shortage for parasitized gobies than for those free of parasites. We found interactive effects of refuge shortage and parasitism on two behaviours we predicted might be associated with parasite-mediated competition for refuges. First, as refuge-shortage increases, the rate of aggression among gobies increases and parasitism intensifies this interaction. Second, goby proximity to refuges increases as refuges become scarce, but parasitism nullifies this increase. In combination, these parasite-induced changes in behaviour may explain why parasitized gobies are poor competitors for refuges. Because the parasite is not trophically transmitted via host manipulation, these altered behaviours in parasitized gobies are likely coincidental to infection.