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Abstract
The colonial ascidian Botryllus schlosseri expresses a unique allorecognition system. When two histoincompatible Botryllus colonies come into direct contact, they develop an inflammatory-like rejection response. A surprising high number of vertebrates' coagulation genes and coagulation-related domains were disclosed in a cDNA library of differentially expressed sequence tags (ESTs), prepared for this allorejection process. Serine proteases, especially from the trypsin family, were highly represented among Botryllus library ortholgues and its “molecular function” gene ontology analysis. These, together with the built-up clot-like lesions in the interaction area, led us to further test whether a vertebrate-like clotting system participates in Botryllus innate immunity. Three morphologically distinct clot types (points of rejection; POR) were followed. We demonstrated the specific expression of nine coagulation orthologue transcripts in Botryllus rejection processes and effects of the anti-coagulant heparin on POR formation and heartbeats. In situ hybridization of fibrinogen and von Willebrand factor orthologues elucidated enhanced expression patterns specific to histoincompatible reactions as well as common expressions not augmented by innate immunity. Immunohistochemistry for fibrinogen revealed, in naïve and immune challenged colonies alike, specific antibody binding to a small population of Botryllus compartment cells. Altogether, molecular, physiological and morphological outcomes suggest the involvement of vertebrates-like coagulation elements in urochordate immunity, not assigned with vasculature injury.
Highlights
Blood coagulation, a vital body defense mechanism [1], is a shared vertebrata mechanism that allows an improved management of blood fluidity following vascular injury
Whereas the chordate Amphioxus has a thrombin-like enzyme but no true fibrinogen [5], the solitary urochordate Ciona intestinalis genome did not display any genuine orthologues for the coagulation genes, paralogues and constituent domains had been recorded for virtually all coagulation factors [4]
To avoid variations in the results caused by different onsets of rejection patterns and genotypic specific reactions, rejection classifications were established by analyzing histological sections done on the climax status of the developed POR
Summary
A vital body defense mechanism [1], is a shared vertebrata mechanism that allows an improved management of blood fluidity following vascular injury. The hemostatic feature of coagulation is activated immediately upon injury, as damage to blood vessel walls exposes collagen (normally present under the endothelium), to which circulating platelets bind through specific surface receptors. This adhesion is further strengthened by the von Willebrand factor (vWF) circulating protein, which forms links between platelet glycoproteins and collagen fibrils, ensuring the formation of primary hemostatic plug. This analysis confirmed earlier studies on the solitary ascidian Halocynthia roretzi, suggesting the absence of the vertebrates’ coagulation system in its hemolymph [6], while featuring a thrombin-like serine protease that can convert mammalian fibrinogen to fibrin, producing a clot [7]
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