Three distinct RNAs for the surface protease gp63 are differentially expressed during development of Leishmania donovani chagasi promastigotes to an infectious form.

Ramamoorthy, Ramesh; Donelson, John E.; Paetz, K. E.; Maybodi, M; Roberts, Sigrid C.; Wilson, Mary E.

doi:10.1016/s0021-9258(18)46030-9

Cited by 122 publications

(6 citation statements)

References 53 publications

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“…However, we have not ruled out the possibility that the cleaved peptide was too small to produce a shift in the mobility of secreted gp63. Lastly, we note reports that L. donovani chagasi and L. mexicana express gp63 transcripts that do not have GPI addition signals (47,58,73). If such proteins were present in L. major and were membrane bound, their cell association will not be expected to be affected by GPI-PLC.…”

Section: Gp63 Is Secreted Without Prior Addition Of a Gpi Anchormentioning

confidence: 85%

A glycosylphosphatidylinositol (GPI)-negative phenotype produced in Leishmania major by GPI phospholipase C from Trypanosoma brucei: topography of two GPI pathways

Mensa-Wilmot

LeBowitz

Chang

et al. 1994

The Journal of Cell Biology

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Abstract. The major surface macromolecules of the protozoan parasite Leishmania major, gp63 (a metalloprotease), and lipophosphoglycan (a polysaccharide), are glycosylphosphatidylinositol (GPI) anchored. We expressed a cytoplasmic glycosylphosphatidylinositol phospholipase C (GPI-PLC) in L. major in order to examine the topography of the protein-GPI and polysaccharide-GPI pathways. In L. major cells expressing GPI-PLC, cell-associated gp63 could not be detected in immunoblots. Pulse-chase analysis revealed that gp63 was secreted into the culture medium with a half-time of 5.5 h. Secreted gp63 lacked anti-cross reacting determinant epitopes, and was not metabolically labeled with [3H]ethanolamine, indicating that it never received a GPI anchor. Further, the quantity of putative protein-GPI intermediates decreased ,,ol0-fold. In striking contrast, lipophosphoglycan levels were unaltered. However, GPI-PLC cleaved polysaccharide-GPI intermediates (glycoinositol phospholipids) in vitro. Thus, reactions specific to the polysaccharide-GPI pathway are comparianentalized in vivo within the endoplasmic reticulum, thereby sequestering polysaccharide-GPI intermediates from GPI-PLC cleavage. On the contrary, protein-GPI synthesis at least up to production of Man(lat)Man(lot4)GlcN-(lat)-myo-inositol-l-phospholipid is cytosolic. To our knowledge this represents the first use of a catabolic enzyme in vivo to elucidate the topography of biosynthetic pathways.GPI-PLC causes a protein-GPI-negative phenotype in L. major, even when genes for GPI biosynthesis are functional. This phenotype is remarkably similar to that of some GPI mutants of mammalian cells: implications for paroxysmal nocturnal hemoglobinuria and Thy-l-negative T-lymphoma are discussed. LYCOSYLPHOSPHATIDYLINOSITOL (GP1) t anchors attach a diverse group of macromolecules to membranes in eukaryotes (see 19, 22 for recent reviews). The plasma membrane of the protozoan parasite Trypmwsoma brucei is covered with about 107 molecules of the variant surface glycoprotein (VSG), a GPI-anchored molePlease address all correspondence to Dr. K. Mensa-Wilmot, Department of Zoology, University of Georgia, Athens, Georgia 30602.1. Abbreviations used in this paper: CRD, cross-reacting determinant; dol-P-Man, dolichol-phosphoryl-mannose; eGPI-PLC, recombinant glycosylphosphatidylinositol phospholipase C; EtN, ethanolamine; gp63, 63-kD GPI-anchored glycoprotein of Leishmania parasites; GIPL, glycoinositol phospholipid; GPI, glycosylphosphatidylinositol; GPI-PLC, glycosylphosphatidylinositol phospholipnse C; Gall, Galactofuranose; GleN, glucosamine; GIcNAC, N-acetyl glucosamine; LP-1, putative protein-GPI precursor (possibly EtN-phospho-ManrGlcN-PI); LP-2, putative protein-GPl precursor; LPG, lipophosphoglycan; Man, mannose; mfVSG, membraneform VSG; PI, phosphatidylinositol; PNH, paroxysmal nocturnal hemoglobinuria; UDP-GIcNAc, uridine 5'-diphospho N-acetylglucosamine; VSG, variant surface glycoprotein of Trypanosoma brucei.cule. The VSG GPI consists of dimyristoylphosphatidylinositol l...

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Section: Gp63 Is Secreted Without Prior Addition Of a Gpi Anchormentioning

confidence: 85%

A glycosylphosphatidylinositol (GPI)-negative phenotype produced in Leishmania major by GPI phospholipase C from Trypanosoma brucei: topography of two GPI pathways

Mensa-Wilmot

LeBowitz

Chang

et al. 1994

The Journal of Cell Biology

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“…All Leishmania sp. inspected have numerous tandem genes encoding gp63 ( 26 , 27 ). Gp63 in ten Leishmania sp.…”

Section: Introductionmentioning

confidence: 99%

Major Molecular Factors Related to Leishmania Pathogenicity

Al-Khalaifah

2022

Front. Immunol.

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Leishmaniasis is a major health problem with 600k - 1M new cases worldwide and 1 billion at risk. It involves a wide range of clinical forms ranging from self-healing cutaneous lesions to systemic diseases that are fatal if not treated, depending on the species of Leishmania. Leishmania sp. are digenetic parasites that have two different morphological stages. Leishmania parasites possess a number of invasive/evasive and pathoantigenic determinants that seem to have critical roles in Leishmania infection of macrophages which leads to successful intracellular parasitism in the parasitophorous vacuoles. These determinants are traditionally known as “virulence factors”, and are considered to be good targets for developing specific inhibitors to attenuate virulence of Leishmania by gene deletions or modifications, thus causing infective, but non-pathogenic mutants for vaccination. Pathway of biosynthesis is critical for keeping the parasite viable and is important for drug designing against these parasites. These drugs are aimed to target enzymes that control these pathways. Accordingly, maintaining low level of parasitic infection and in some cases as a weapon to eradicate infection completely. The current paper focuses on several virulence factors as determinants of Leishmania pathogenicity, as well as the metabolites produced by Leishmania to secure its survival in the host.

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“…Πρέπει επίσης να αναφερθεί ότι ο µεγαλύτερος βαθµός ετερογένειας, τόσο στον αριθµό όσο και στην οργάνωση των γονιδίων µεταξύ διαφόρων ειδών Leishmania που µελετήθηκαν, παρατηρείται σε γενετικούς τόπους που περιέχουν γονίδια αντιγόνων επιφανείας (π.χ. gp63), (Ramamoorthy et al, 1992).…”

Section: γονιδιακή οργάνωσηunclassified

Μελέτη του βιολογικού ρόλου της ιστόνης Η1 και της κινάσης της συνθετάσης του γλυκογόνου (GSK-3) της Leishmania

Xingi¹,

Ξύγγη²

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Μελέτη του βιολογικού ρόλου της ιστόνης Η1 και της κινάσης της συνθετάσης του γλυκογόνου (GSK-3) της Leishmania ΞΥΓΓΗ ΕΥΑΓΓΕΛΙΑ ΠΑΝΕΠΙΣΤΗΜΙΟ ΚΡΗΤΗΣ ΤΜΗΜΑ ΙΑΤΡΙΚΗΣ EΡΓΑΣΤΗΡΙΟ ΚΛΙΝΙΚΗΣ ΒΑΚΤΗΡΙΟΛΟΓΙΑΣ, ΠΑΡΑΣΙΤΟΛΟΓΙΑΣ, ΖΩΟΝΟΣΩΝ ΚΑΙ ΓΕΩΓΡΑΦΙΚΗΣ ΙΑΤΡΙΚΗΣ ΕΛΛΗΝΙΚΟ ΙΝΣΤΙΤΟΥΤΟ ΠΑΣΤΕΡ ΤΜΗΜΑ ΜΙΚΡΟΒΙΟΛΟΓΙΑΣ ΕΡΓΑΣΤΗΡΙΟ ΜΟΡΙΑΚΗΣ ΠΑΡΑΣΙΤΟΛΟΓΙΑΣ ∆Ι∆ΑΚΤΟΡΙΚΗ ∆ΙΑΤΡΙΒΗ ΚΡΗΤΗ 2009 4.5 Επιδράσεις της υπερέκφρασης της LdGSK-3short στα L. donovani προµαστιγωτά..

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Three distinct RNAs for the surface protease gp63 are differentially expressed during development of Leishmania donovani chagasi promastigotes to an infectious form.

Cited by 122 publications

References 53 publications

A glycosylphosphatidylinositol (GPI)-negative phenotype produced in Leishmania major by GPI phospholipase C from Trypanosoma brucei: topography of two GPI pathways

A glycosylphosphatidylinositol (GPI)-negative phenotype produced in Leishmania major by GPI phospholipase C from Trypanosoma brucei: topography of two GPI pathways

Major Molecular Factors Related to Leishmania Pathogenicity

Μελέτη του βιολογικού ρόλου της ιστόνης Η1 και της κινάσης της συνθετάσης του γλυκογόνου (GSK-3) της Leishmania

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