Surface Anionic Groups in Symbiote‐Bearing and Symbiote‐Free Strains ofCrithidia deanei¹

Abstract

The surface anionic groups of symbiote‐bearing and symbiote‐free strains of Crithidia deanei were compared by determining cellular electrophoretic mobility, by ultrastructural cytochemistry, and by identification of sialic acids by thin‐layer and gasliquid chromatography. Symbiote‐free Crithidia deanei has a highly negative surface charge (‐0.9984 μmċs‐1ċ V‐1ċ cm), which is slightly reduced (‐0.8527 μmċs‐1ċ V‐1ċ cm) by the presence of the endosymbiote. Treatment of both strains of C. deanei with neuraminidase decreased significantly the electrophoretic mobility of cells toward the cathodic pole, indicating the existence of exposed sialic acid residues responsible for the negative charge on the protozoan cell surface. Thin‐layer and gas‐liquid chromatography showed that N‐glycolyl‐ and N‐acetylneuraminic acids were present in both strains of C. deanei.

Endosymbiosis in protozoa of the Trypanosomatidae family

“…The presence of the endosymbiont also interferes with surface properties of the protozoan, such as: (a) exposition of carbohydrate residues, as evaluated by interaction with lectins [30^32] and by identi¢cation of membrane-associated polysaccharides using gasl iquid chromatography [33]; and (b) the surface charge, as evaluated by the binding of cationic particles to the protozoan surface and direct measurement of its electrophoretic mobility [34].…”

The surface charge of trypanosomatids

“…Crithidia deanei is known to harbor endosymbiotic bacterium-like organism that is integrated into the physiology of the host cell (McGhee and Cosgrove 1980). Although symbiote-bearing and symbiote-free strains of C. deanei presented a negative cell surface charge due to the presence of sialic acid, no significant binding of CIH was observed and binding of CF to the surface of both strains was not observed (Oda et al 1984). Binding of CF particles was observed on the cell surface of Crithidia luciliae and of both wild and drug-resistant mutant strains of Crithidia fasciculata.…”

“…The possibility of elimination of the endosymbiont by the use of antibiotics has increased the interest in the study of endosymbiont-harboring species. The available data indicate that the presence of the endosymbiont induces morphological changes, as the lack of paraflagellar structure located in the flagellum (Freymüller and Camargo 1981) interferes with the metabolism of the trypanosomatid (Newton 1957, Mundim et al 1974, Alfieri and Camargo 1982, Salzman et al 1985, De Souza and Motta 1999, diminishes the secretion of proteolytic enzymes (d'Avila-Levy et al 2001), interferes with surface properties of the protozoan such as exposition of carbohydrate residues (Dwyer and Chang 1976, Esteves et al 1982, McLaughlin and Cain 1985, Faria e Silva et al 1994) and on the surface charge (Oda et al 1984). Symbiont-free C. deanei presents a mean EPM of −0.99µm.s −1 .V −1 .cm, which is 15% more negative than the symbiont-free strain.…”

“…Cell surface charge of three species of the genus Crithidia was analyzed by determining the cellular electrophoretic mobility, ultrastructural cytochemistry, thin layer and gas liquid chromatography, lectin agglutinations assays and enzymatic treatments. Crithidia deanei, C. fasciculata and C. luciliae have a net negative cell surface charge (Table I) ( Oda et al 1984, Matta et al 1992. Treatment of these strains with neuraminidase from C. perfringens only reduced significantly the EPM of C. deanei.…”

“…Symbiont-free C. deanei presents a mean EPM of −0.99µm.s −1 .V −1 .cm, which is 15% more negative than the symbiont-free strain. Treatment of C. deanei with neuraminidase reduced in about 45% the EPM of the protozoan, irrespective of the presence of the endosymbiote (Oda et al 1984). Parasites of the genus Herpetomonas have been used to analyze changes on cell surface during the process of differentiation in vitro, since the composition of the plasma membrane and the surface coat are of primary importance in cell response to environmental stimuli and in the interaction of parasites with their hosts (Soares et al 1988, Lopes et al 1989, Faria-e-Silva et al 1999.…”