Abstract
Biomphalaria glabrata is a freshwater Planorbidae snail. In its environment, this mollusk faces numerous microorganisms or pathogens, and has developed sophisticated innate immune mechanisms to survive. The mechanisms of recognition are quite well understood in Biomphalaria glabrata, but immune effectors have been seldom described. In this study, we analyzed a new family of potential immune effectors and characterized five new genes that were named Glabralysins. The five Glabralysin genes showed different genomic structures and the high degree of amino acid identity between the Glabralysins, and the presence of the conserved ETX/MTX2 domain, support the hypothesis that they are pore-forming toxins. In addition, tertiary structure prediction confirms that they are structurally related to a subset of Cry toxins from Bacillus thuringiensis, including Cry23, Cry45, and Cry51. Finally, we investigated their gene expression profiles in snail tissues and demonstrated a mosaic transcription. We highlight the specificity in Glabralysin expression following immune stimulation with bacteria, yeast or trematode parasites. Interestingly, one Glabralysin was found to be expressed in immune-specialized hemocytes, and two others were induced following parasite exposure.
Highlights
All living organisms are confronted with environments full of complex changing populations of microorganisms and potential pathogens, engendering strong selective pressures that drive the complexification and evolution of their immune system [1,2,3]
The first step consists of pattern recognition through microbe-associated molecular patterns (MAMPs), pathogen associated molecular patterns (PAMPs), or damage-associated molecular patterns (DAMPs) [4,5,6,7]
In the present study we investigated the presence of putative new -pore-forming toxin family members from the snail B. glabrata
Summary
All living organisms are confronted with environments full of complex changing populations of microorganisms and potential pathogens, engendering strong selective pressures that drive the complexification and evolution of their immune system [1,2,3]. The innate immune reactions mounted to recognize and control/contain and/or eliminate microbe or parasite infections is considered to be subdivided into three steps. The second one consists of signaling pathways that regulate and control the activation of the immune response triggering the third step that consists of the production and release of effector molecules dedicated to pathogen killing [3]. The Planorbidae snail Biomphalaria glabrata (B. glabrata), constitutes an original model for studying such responses. B. glabrata snails face in their environment, viruses [8], bacteria [9], protozoa [10], yeast [11] nematodes [12] and various trematodes. Biomphalaria sp. is mainly known for its role as vector snail of the human schistosomiasis disease for which the trematode Schistosoma sp. is the etiological agent, but the snail acts as an intermediate host for numerous Echinostoma trematode species [13]
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