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Seed dispersal and burial are important processes in the expansion and restoration of Zostera marina (eelgrass) meadows. The depth at which seeds are buried is a significant factor contributing to the success of seedling survival. If seeds are buried below 6 cm, it is unlikely that viable seedlings will develop, while shallow burials protect seeds from predation on the sediment surface. Burrowing behavior of infaunal organisms is one factor that contributes to seed burial with a potentially positive or negative influence on seedling survival. In this study, we designed a laboratory experiment to determine the relationship between lugworm (Abarenicola pacifica) density and eelgrass seed burial. Three treatments (no worms, low-density, and high-density of worms) with three replicates each were used to quantify seed burial. Each replicate was seeded with a blend of seed mimics and real seeds. After 25 days, three cores were extracted from each replicate and the depths of the seeds recorded. In the high-density worm treatments, most of the seeds and mimics were buried below the 6 cm critical depth, while in the low-density treatments most seeds were found shallower than 3 cm. These results agree with previous work on the burying capacity of infaunal organisms, and strongly suggest that the presence and activity of infauna can determine the success of Z. marina meadow expansion and restoration. [ABSTRACT FROM AUTHOR]

Background: Spotting disease infects a variety of sea urchin species across many different marine locations. The disease is characterized by discrete lesions on the body surface composed of discolored necrotic tissue that cause the loss of all surface appendages within the lesioned area. A similar, but separate disease of sea urchins called bald sea urchin disease (BSUD) has overlapping symptoms with spotting disease, resulting in confusions in distinguishing the two diseases. Previous studies have focus on identifying the underlying causative agent of spotting disease, which has resulted in the identification of a wide array of pathogenic bacteria that vary based on location and sea urchin species. Our aim was to investigate the spotting disease infection by characterizing the microbiomes of the animal surface and various tissues. Results: We collected samples of the global body surface, the lesion surface, lesioned and non-lesioned body wall, and coelomic fluid, in addition to samples from healthy sea urchins. 16S rRNA gene was amplified and sequenced from the genomic DNA. Results show that the lesions are composed mainly of Cyclobacteriaceae, Cryomorphaceae, and a few other taxa, and that the microbial composition of lesions is the same for all infected sea urchins. Spotting disease also alters the microbial composition of the non-lesioned body wall and coelomic fluid of infected sea urchins. In our closed aquarium systems, sea urchins contracted spotting disease and BSUD separately and therefore direct comparisons could be made between the microbiomes from diseased and healthy sea urchins. Conclusion: Results show that spotting disease and BSUD are separate diseases with distinct symptoms and distinct microbial compositions. [ABSTRACT FROM AUTHOR]

Background: Spotting disease infects a variety of sea urchin species across many different marine locations. The disease is characterized by discrete lesions on the body surface composed of discolored necrotic tissue that cause the loss of all surface appendages within the lesioned area. A similar, but separate disease of sea urchins called bald sea urchin disease (BSUD) has overlapping symptoms with spotting disease, resulting in confusions in distinguishing the two diseases. Previous studies have focus on identifying the underlying causative agent of spotting disease, which has resulted in the identification of a wide array of pathogenic bacteria that vary based on location and sea urchin species. Our aim was to investigate the spotting disease infection by characterizing the microbiomes of the animal surface and various tissues. Results: We collected samples of the global body surface, the lesion surface, lesioned and non-lesioned body wall, and coelomic fluid, in addition to samples from healthy sea urchins. 16S rRNA gene was amplified and sequenced from the genomic DNA. Results show that the lesions are composed mainly of Cyclobacteriaceae, Cryomorphaceae, and a few other taxa, and that the microbial composition of lesions is the same for all infected sea urchins. Spotting disease also alters the microbial composition of the non-lesioned body wall and coelomic fluid of infected sea urchins. In our closed aquarium systems, sea urchins contracted spotting disease and BSUD separately and therefore direct comparisons could be made between the microbiomes from diseased and healthy sea urchins. Conclusion: Results show that spotting disease and BSUD are separate diseases with distinct symptoms and distinct microbial compositions. [ABSTRACT FROM AUTHOR]

The vertebrate complement cascade is an essential host protection system that functions at the intersection of adaptive and innate immunity. However, it was originally assumed that complement was present only in vertebrates because it was activated by antibodies and functioned with adaptive immunity. Subsequently, the identification of the key component, SpC3, in sea urchins plus a wide range of other invertebrates significantly expanded the concepts of how complement functions. Because there are few reports on the echinoid complement system, an alternative approach to identify complement components in echinoderms is to search the deduced proteins encoded in the genomes. This approach identified known and putative members of the lectin and alternative activation pathways, but members of the terminal pathway are absent. Several types of complement receptors are encoded in the genomes. Complement regulatory proteins composed of complement control protein (CCP) modules are identified that may control the activation pathways and the convertases. Other regulatory proteins without CCP modules are also identified, however regulators of the terminal pathway are absent. The expansion of genes encoding proteins with Macpf domains is noteworthy because this domain is a signature of perforin and proteins in the terminal pathway. The results suggest that the major functions of the echinoid complement system are detection of foreign targets by the proteins that initiate the activation pathways resulting in opsonization by SpC3b fragments to augment phagocytosis and destruction of the foreign targets by the immune cells. • Proteins encoded in the Strongylocentrotus purpuratus genome identifies the lectin and alternative pathways of complement. • Associated serine proteases of the lectin pathway are absent in echinoids but identified in asteroids. • The terminal pathway is missing and may be replaced by an expansion of Macpf-containing proteins. • Many proteins with multiple CCP modules may have regulatory functions. • The major activity of the complement system in echinoids may be opsonization. [ABSTRACT FROM AUTHOR]