Novel Kunitz-like Peptides Discovered in the Zoanthid Palythoa caribaeorum through Transcriptome Sequencing.

Palythoa caribaeorum (class Anthozoa) is a zoanthid that together jellyfishes, hydra, and sea anemones, which are venomous and predatory, belongs to the Phyllum Cnidaria. The distinguished feature in these marine animals is the cnidocytes in the body tissues, responsible for toxin production and injection that are used majorly for prey capture and defense. With exception for other anthozoans, the toxin cocktails of zoanthids have been scarcely studied and are poorly known. Here, on the basis of the analysis of P. caribaeorum transcriptome, numerous predicted venom-featured polypeptides were identified including allergens, neurotoxins, membrane-active, and Kunitz-like peptides (PcKuz). The three predicted PcKuz isotoxins (1-3) were selected for functional studies. Through computational processing comprising structural phylogenetic analysis, molecular docking, and dynamics simulation, PcKuz3 was shown to be a potential voltage gated potassium-channel inhibitor. PcKuz3 fitted well as new functional Kunitz-type toxins with strong antilocomotor activity as in vivo assessed in zebrafish larvae, with weak inhibitory effect toward proteases, as evaluated in vitro. Notably, PcKuz3 can suppress, at low concentration, the 6-OHDA-induced neurotoxicity on the locomotive behavior of zebrafish, which indicated PcKuz3 may have a neuroprotective effect. Taken together, PcKuz3 figures as a novel neurotoxin structure, which differs from known homologous peptides expressed in sea anemone. Moreover, the novel PcKuz3 provides an insightful hint for biodrug development for prospective neurodegenerative disease treatment.

Toxic potential of palytoxin.

This review briefly describes the origin, chemistry, molecular mechanism of action, pharmacology, toxicology, and ecotoxicology of palytoxin and its analogues. Palytoxin and its analogues are produced by marine dinoflagellates. Palytoxin is also produced by Zoanthids (i.e. Palythoa), and Cyanobacteria (Trichodesmium). Palytoxin is a very large, non-proteinaceous molecule with a complex chemical structure having both lipophilic and hydrophilic moieties. Palytoxin is one of the most potent marine toxins with an LD50 of 150 ng/kg body weight in mice exposed intravenously. Pharmacological and electrophysiological studies have demonstrated that palytoxin acts as a hemolysin and alters the function of excitable cells through multiple mechanisms of action. Palytoxin selectively binds to Na(+)/K(+)-ATPase with a Kd of 20 pM and transforms the pump into a channel permeable to monovalent cations with a single-channel conductance of 10 pS. This mechanism of action could have multiple effects on cells. Evaluation of palytoxin toxicity using various animal models revealed that palytoxin is an extremely potent neurotoxin following an intravenous, intraperitoneal, intramuscular, subcutaneous or intratracheal route of exposure. Palytoxin also causes non-lethal, yet serious toxic effects following dermal or ocular exposure. Most incidents of palytoxin poisoning have manifested after oral intake of contaminated seafood. Poisonings in humans have also been noted after inhalation, cutaneous/systemic exposures with direct contact of aerosolized seawater during Ostreopsis blooms and/or through maintaining aquaria containing Cnidarian zoanthids. Palytoxin has a strong potential for toxicity in humans and animals, and currently this toxin is of great concern worldwide.

Gene duplications are extensive and contribute significantly to the toxic proteome of nematocysts isolated from Acropora digitifera (Cnidaria: Anthozoa: Scleractinia).

BACKGROUND: Gene duplication followed by adaptive selection is a well-accepted process leading to toxin diversification in venoms. However, emergent genomic, transcriptomic and proteomic evidence now challenges this role to be at best equivocal to other processess . Cnidaria are arguably the most ancient phylum of the extant metazoa that are venomous and such provide a definitive ancestral anchor to examine the evolution of this trait. METHODS: Here we compare predicted toxins from the translated genome of the coral Acropora digitifera to putative toxins revealed by proteomic analysis of soluble proteins discharged from nematocysts, to determine the extent to which gene duplications contribute to venom innovation in this reef-building coral species. A new bioinformatics tool called HHCompare was developed to detect potential gene duplications in the genomic data, which is made freely available ( https://github.com/rgacesa/HHCompare ). RESULTS: A total of 55 potential toxin encoding genes could be predicted from the A. digitifera genome, of which 36 (65 %) had likely arisen by gene duplication as evinced using the HHCompare tool and verified using two standard phylogeny methods. Surprisingly, only 22 % (12/55) of the potential toxin repertoire could be detected following rigorous proteomic analysis, for which only half (6/12) of the toxin proteome could be accounted for as peptides encoded by the gene duplicates. Biological activities of these toxins are dominatedby putative phospholipases and toxic peptidases. CONCLUSIONS: Gene expansions in A. digitifera venom are the most extensive yet described in any venomous animal, and gene duplication plays a significant role leading to toxin diversification in this coral species. Since such low numbers of toxins were detected in the proteome, it is unlikely that the venom is evolving rapidly by prey-driven positive natural selection. Rather we contend that the venom has a defensive role deterring predation or harm from interspecific competition and overgrowth by fouling organisms. Factors influencing translation of toxin encoding genes perhaps warrants more profound experimental consideration.

Status of aspergillosis and sea fan populations in Curaçao ten years after the 1995 Caribbean epizootic / Situación de las poblaciones de aspergilosis y abanicos de mar en Curazao diez años después de la epizootia del Caribe de 1995

In 1995, a survey of sea fan corals was conducted in Curaçao during a Caribbean-wide outbreak of the sea fan disease aspergillosis. The survey was repeated in 2005 using the same methodology and identical sites to examine changes in sea fan populations 10 years after the initial epizootic. Necrotic lesions typical of aspergillosis were present on as many sea fans in 2005 as in 1995 (mean ± SE: 52 ± 6 vs 43 ± 10%). The disease also showed no significant variation in virulence (9.6 ± 1.2 vs 8.8 ± 1.0% tissue loss per diseased colony). However, the average number of sea fan colonies per 10 m² decreased from 2.7 ± 1.1 to 0.7 ± 0.2 over the 10-year period, a decline of almost 75%. This decrease occurred for all colony sizes, but was more pronounced among small colonies, resulting in an overall trend of domination by large colonies. These results support that aspergillosis can have a significant, long-term impact on sea fan population size and structure. The continued presence of the disease in 2005 could be contributing to reduced recruitment and/or selective mortality among the smallest colonies. This study provides no indication that host resistance against aspergillosis could reverse the decline of Caribbean sea fan corals. Rev. Biol. Trop. 54 (Suppl. 3): 153-160. Epub 2007 Jan. 15.

En 1995, se realizó un sondeo de los abanicos de mar durante un brote de aspergilosis, una enfermedad de abanicos de mar extendida en todo el Caribe. En el año 2005 se repitió el sondeo utilizando exactamente la misma metodología y los mismos sitios para examinar cambios en las poblaciones tras 10 años del inicio del brote. Se presentaron lesiones necróticas típicas de la aspergilosis en tantos abanicos en el 2005, como en 1995 (promedio ± ES: 52 ± 6 vs 43 ± 10%). La enfermedad tampoco mostró variaciones significativas en la virulencia (9.6 ± 1.2 vs 8.8 ± 1.0%, pérdida de tejido por colonia enferma). Sin embargo, el número promedio de colonias de abanico de mar por cada 10 m² bajó desde 2.7 ± 1 hasta 0.7 ± 0.2 en este período de 10 años, una disminución de casi 75%. Este decrecimiento ocurrió en colonias de todo tamaño, pero fue más pronunciado en colonias pequeñas, produciendo una tendencia general de dominancia de colonias grandes. Estos resultados apoyan la idea de que la aspergilosis puede tener un impacto significativo a largo plazo en el tamaño y estructura poblacional de los abanicos de mar. La continuidad en la presencia de la enfermedad en el 2005 puede estar contribuyendo a la reducción en el reclutamiento y/o a la mortalidad selectiva de las colonias más pequeñas. Este estudio no provee ninguna evidencia de que la resistencia del hospedero contra la aspergilosis pueda revertir el decrecimiento de los abanicos de mar en el Caribe.

Picadura por coral de fuego / Bite by fire choral

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