A lytic mechanism based on soluble phospholypases A2 (sPLA2) and β-galactoside specific lectins is exerted by Ciona intestinalis (ascidian) unilocular refractile hemocytes against K562 cell line and mammalian erythrocytes

Routes in Innate Immunity Evolution: Galectins and Rhamnose‐binding Lectins in Ascidians

“…Vizzini et al (2011) analyzed the sequenced cDNA and CRD sequences and supported the predicted bi-CRD CiLgals-a and CiLgals-b gene organization and the chromosome localization (chromosome 4q and chromosome 6q, respectively). The CiLgals-a transcript (1285 nt) encodes a 289-amino acid sequence with a deduced molecular size of 32 kDa, and the CiLgals-b transcript (1332 nt) encodes a 318-amino acid sequence (37 kDa).…”

“…Interestingly, a B. schlosseri lectin type contains both a C-type lectin domain and an immunoglobulin-like domain (Pancer et al, 1997), similar to the fibrinogen-related proteins from molluscs (FREPS) involved in defense (Adema et al, 1997). Finally, a lytic mechanism based on soluble phospholypases A2 (sPLA2) and β-galactoside-specific lectins is exerted by C. intestinalis hemocytes against the K562 cell line and mammalian erythrocytes (Arizza et al, 2011).…”

“…The CiLgals-a transcript (1285 nt) encodes a 289-amino acid sequence with a deduced molecular size of 32 kDa, and the CiLgals-b transcript (1332 nt) encodes a 318-amino acid sequence (37 kDa). Like vertebrate cytosolic galectins, they do not contain a signal peptide and presumably are released through a nonclassical secretory pathway (Vizzini et al, 2011). The major sequence-similarity and identity percentages were found with chicken galectin 8 (CiLgals-a) and mouse galectin 6 (CiLgals-b).…”

“…Otherwise, the CiLgal-b presents a specific F4-CRD-linker-F4-CRD organization. Moreover, the CiLgals-a and CiLgals-b CRD sequences were aligned with F4-CRD-linkers-F3-CRD vertebrate bi-CRD galectins, the cephalochordate Branchiostoma floridae, the echinoderm Strongylocentrotus purpuratus gal RL30 galectin and the ascidian Clavelina picta mono-CRD gal16 (Vizzini et al, 2011). The phylogenetic tree shows that vertebrate N-CRDs and C-CRDs are grouped into two distinct clusters, indicating an early domain divergence after a duplication event.…”

Upregulated transcription of phenoloxidase genes in the pharynx and endostyle of Ciona intestinalis in response to LPS

“…The ascidian POs are copperdependent orthodiphenoloxidases (Kahn, 1985;Sugumaran et al, 1988) that were at first identified by histochemical reaction in the tunic hemocytes (Barrington and Thorpe, 1968), suggesting a quinone-tanning system involved in the production of tunic scleroprotein (Chaga, 1980). Circulating hemocytes from naïve ascidians can exert in vitro PO-dependent cytotoxic activity versus erythrocytes and tumor cell lines (Cammarata et al, 1997;Arizza et al, 2011), whereas LPS inoculation activates the proPO pathway, and enhanced PO activity (Jackson et al, 1993;Cammarata and Parrinello, 2009). In non-fusion reaction of colonial ascidians, the enzyme mediates the formation of the cytotoxic foci along the contacting regions of genetically incompatible colonies (Hirose et al, 1990;Ballarin et al, 1998;Shirae and Saito, 2000;Shirae et al, 2002;Cima et al, 2004;Zaniolo et al, 2006).…”