Organization of trans-sialidase genes in Trypanosoma cruzi

Egima, Claudia M.; Briones, Marcelo R. S.; Freitas, Lucio H.G de; Schenkman, Rocilda P.F.; Uemura, Hirotsugu; Schenkman, Sérgio

doi:10.1016/0166-6851(96)02582-0

Cited by 25 publications

(15 citation statements)

References 27 publications

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“…The host cell receptors for many of these ligands have not yet been identified. Many members (gp82, gp90, gp85/TS, gp30) of the gp85/trans-sialidase (TS) super-family are implicated in the initiation of infection by trypomastigotes[102, 103]. Gp82, and the related gp30, are MT-specific surface proteins that upon engagement of an unknown receptor(s) mediate bidirectional Ca 2+ release in both the parasite and host cell[104–106].…”

Section: Mechanisms Of Host Cell Invasion By Trypanosoma Cruzimentioning

confidence: 99%

Mechanisms of cellular invasion by intracellular parasites

Walker

Oghumu

Gupta

et al. 2013

Cell. Mol. Life Sci.

146

108

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Numerous disease-causing parasites must invade host cells to prosper. Collectively, such pathogens are responsible for a staggering amount of human sickness and death throughout the world. Leishmaniasis, Chagas disease, toxoplasmosis, and malaria are neglected diseases and therefore are linked to socio-economical and geographical factors, affecting well-over half the world's population.Such obligate intracellular parasites have co-evolved with humans to establish a complexity of specific molecular parasite-host cell interactions, forming the basis of the parasite's cellular tropism. They make use of such interactions to invade host cells as a means to migrate through various tissues, to evade the host immune system, and to undergo intracellular replication. These cellular migration and invasion events are absolutely essential for the completion of the lifecycles of these parasites and lead to their for disease pathogenesis.This review is an overview of the molecular mechanisms of protozoan parasite invasion of host cells and discussion of therapeutic strategies, which could be developed by targeting these invasion pathways. Specifically, we focus on four species of protozoan parasites

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Section: Mechanisms Of Host Cell Invasion By Trypanosoma Cruzimentioning

confidence: 99%

Mechanisms of cellular invasion by intracellular parasites

Walker

Oghumu

Gupta

et al. 2013

Cell. Mol. Life Sci.

146

108

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“…The genes of the TS family encode for the unique pathogen-derived surface sialidase, the active TS (aTS), which transfers a2,3-linked sialic acid to terminal b-galactopyranose residues (bGalp) (Previato et al, 1985) and for its inactive analogue (iTS). iTS has a His at position 342, while active members express a Tyr at the same position (Cremona et al, 1995;Egima et al, 1996). The group of TS-like genes encodes for molecules displaying about 30% homology to active TS and includes the gp85/TS glycoproteins (Giordano et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Endothelial cell signalling induced by trans-sialidase from Trypanosoma cruzi

et al. 2007

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SummaryThe protozoan responsible for Chagas' disease, Trypanosoma cruzi, expresses on its surface an unusual trans-sialidase enzyme thought to play an important role in host-parasite interactions. Trans-sialidase is the product of a multigene family encoding both active and inactive proteins. We have demonstrated that despite lacking enzymatic activity due to a single mutation, Tyr342-His, inactive trans-sialidase displays sialic acid binding activity, with identical specificity to that of its active analogue. In this work we demonstrate that binding of a recombinant inactive trans-sialidase to molecules containing a2,3-linked sialic acid on endothelial cell surface triggers NF-kB activation, expression of adhesion molecules and upregulation of parasite entry into host cells. Furthermore, inactive recombinant trans-sialidase blocks endothelial cell apoptosis induced by growth factor deprivation. These results suggest that inactive members of the trans-sialidase family play a role in endothelial cell responses to T. cruzi infection.

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“…2 Several pieces of evidence suggest that TS is involved in cell invasion (35) and escape from the phagosome (36) and is an important virulence factor mediating the immune response to the parasite in the mammalian host (37,38). TS is encoded by a family of ϳ80 genes that have a common amino-terminal domain, which includes the catalytic portion of the enzyme, and a variable number of 12-amino acid repeats in the carboxylterminal region (39).…”

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confidence: 99%

Expression of trans-Sialidase and 85-kDa Glycoprotein Genes in Trypanosoma cruzi Is Differentially Regulated at the Post-transcriptional Level by Labile Protein Factors

Abuin¹,

Freitas‐Junior²,

Colli³

et al. 1999

Journal of Biological Chemistry

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To adapt to different environments, Trypanosoma cruzi, the protozoan parasite that causes Chagas' disease, expresses a different set of proteins during development. To begin to understand the mechanism that controls this differential gene expression, we have analyzed the levels of amastin and trans-sialidase mRNAs and the mRNAs encoding members of the 85-kDa glycoprotein gene family, which are differentially expressed in the T. cruzi stages found in the mammalian host. Amastin mRNA is expressed predominantly in intracellular and proliferative amastigotes. trans-Sialidase mRNAs are found mostly in forms undergoing transformation from amastigotes to trypomastigotes inside infected cells, whereas mRNAs encoding the 85-kDa glycoproteins appear only in the infective trypomastigotes released from the cells. The genes coding for these mRNA species are constitutively transcribed in all stages of T. cruzi cells, suggesting that expression is controlled post-transcriptionally during differentiation. Inhibition of transcription by actinomycin D revealed that each mRNA species has a relatively long half-life in stages where it accumulates. In the case of the transsialidase and 85-kDa glycoprotein genes, mRNA accumulation was induced by treatment with the protein synthesis inhibitor cycloheximide at the stages that preceded the normal accumulation. Therefore, mRNA stabilization may account for mRNA accumulation. mRNA degradation could be promoted by proteins with high turnover, or stabilization could be promoted by forming a complex with the translational machinery at defined times in development. Identification of the factors that induce mRNA degradation or stabilization is essential to the understanding of control of gene expression in these organisms.Gene expression in Trypanosoma cruzi as well as in other trypanosomes is largely controlled at the post-transcriptional level (1-6), although there are a few exceptions where promoters and transcriptional activation have been described (7). Well defined RNA polymerase II initiation sites have not been found, and most genes are transcribed as part of polycistronic units and are processed by trans-splicing (8, 9). During processing, capped spliced leader sequence is added to the 5Ј-end, and a polyadenosine tail is added to the 3Ј-end of mRNA (10), probably ensuring mRNA stability and transport to the cytoplasm (11). In particular, correct splicing and polyadenylation, as well as the existence of specific 3Ј-untranslated portions of the transcribed genes, have been shown to promote either mRNA stability (12) or an increase in the translational efficiency (13). However, the nature of controlling factors and how environmental modifications induce differential expression remain obscure.T. cruzi provides an attractive model to study how modifications in the environment induce differential gene expression. In the insect host, the epimastigote form of the parasite proliferates in the gut. In the posterior gut, where the nutrients become scarce, the parasite transforms into metacyclic ...

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Organization of trans-sialidase genes in Trypanosoma cruzi

Cited by 25 publications

References 27 publications

Mechanisms of cellular invasion by intracellular parasites

Mechanisms of cellular invasion by intracellular parasites

Endothelial cell signalling induced by trans-sialidase from Trypanosoma cruzi

Expression of trans-Sialidase and 85-kDa Glycoprotein Genes in Trypanosoma cruzi Is Differentially Regulated at the Post-transcriptional Level by Labile Protein Factors

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