Cnidaria are venomous animals that produce diverse protein and polypeptide toxins, stored and delivered into the prey through the stinging cells, the nematocytes. These include pore-forming cytolytic toxins such as well studied actinoporins. In this work, we have shown that the non-nematocystic paralytic toxins, hydralysins, from the green hydra Chlorohydra viridissima comprise a highly diverse group of -pore-forming proteins, distinct from other cnidarian toxins but similar in activity and structure to bacterial and fungal toxins. Functional characterization of hydralysins reveals that as soluble monomers they are rich in -structure, as revealed by far UV circular dichroism and computational analysis. Hydralysins bind erythrocyte membranes and form discrete pores with an internal diameter of ϳ1.2 nm. The cytolytic effect of hydralysin is cell type-selective, suggesting a specific receptor that is not a phospholipid or carbohydrate. Multiple sequence alignment reveals that hydralysins share a set of conserved sequence motifs with known pore-forming toxins such as aerolysin, ⑀-toxin, ␣-toxin, and LSL and that these sequence motifs are found in and around the poreforming domains of the toxins. The importance of these sequence motifs is revealed by the cloning, expression, and mutagenesis of three hydralysin isoforms that strongly differ in their hemolytic and paralytic activities. The correlation between the paralytic and cytolytic activities of hydralysin suggests that both are a consequence of receptor-mediated pore formation. Hydralysins and their homologues exemplify the wide distribution of -pore formers in biology and provide a useful model for the study of their molecular mode of action.
In Cnidaria, the production of neurotoxic polypeptides is attributed to the ectodermal stinging cells (cnidocytes), which are discharged for offensive (prey capture) and/or defensive purposes. In this study, a new paralysis-inducing (neurotoxic) protein from the green hydra Chlorohydra Viridissima was purified, cloned, and expressed. This paralytic protein is unique in that it (1) is derived from a noncnidocystic origin, (2) reveals a clear animal group-selective toxicity, (3) possesses an uncommon primary structure, remindful of pore-forming toxins, and (4) has a fast cytotoxic effect on insect cells but not on the tested mammalian cells. The possible biological role of such a noncnidocystic toxin is discussed.
Pore-forming proteins (PFPs) are water-soluble proteins able to integrate into target membranes to form transmembrane pores. They are common determinants of bacterial pathogenicity and are often found in animal venoms. We recently isolated and characterized Hydralysins (Hlns), paralytic PFPs from the venomous green hydra Chlorohydra viridissima that are not found within the nematocytes, suggesting they are not involved in prey capture. The present study aimed to decipher the biological role of Hlns. Using in situ hybridization and immunohistochemistry, we show that Hlns are expressed by digestive cells surrounding the gastrovascular cavity (GVC) of Chlorohydra and secreted onto the prey during feeding. At biologically relevant concentrations, Hlns bind prey membranes and form pores, lysing the cells and disintegrating the prey tissue. Hlns are unable to bind Chlorohydra membranes, thus protecting the producing animal from the destructive effect of its own cytolytic protein. We suggest that osmotic disintegration of the prey within the GVC by Hlns, followed by phagocytosis and intracellular digestion, allows the soft-bodied green hydra to feed on hard, cuticle-covered prey while lacking the physical means to mechanically disintegrate it. Our results extend the biological significance of PFPs beyond the commonly expected offensive or defensive roles.
BackgroundAlgal-cnidarian symbiosis is one of the main factors contributing to the success of cnidarians, and is crucial for the maintenance of coral reefs. While loss of the symbionts (such as in coral bleaching) may cause the death of the cnidarian host, over-proliferation of the algae may also harm the host. Thus, there is a need for the host to regulate the population density of its symbionts. In the green hydra, Chlorohydra viridissima, the density of symbiotic algae may be controlled through host modulation of the algal cell cycle. Alternatively, Chlorohydra may actively expel their endosymbionts, although this phenomenon has only been observed under experimentally contrived stress conditions.Principal FindingsWe show, using light and electron microscopy, that Chlorohydra actively expel endosymbiotic algal cells during predatory feeding on Artemia. This expulsion occurs as part of the apocrine mode of secretion from the endodermal digestive cells, but may also occur via an independent exocytotic mechanism.SignificanceOur results demonstrate, for the first time, active expulsion of endosymbiotic algae from cnidarians under natural conditions. We suggest this phenomenon may represent a mechanism whereby cnidarians can expel excess symbiotic algae when an alternative form of nutrition is available in the form of prey.
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