The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice

In the mammalian host, the cell surface of Trypanosoma brucei is protected by a variant surface glycoprotein that is anchored in the plasma membrane through covalent attachment of the COOH terminus to a glycosylphosphatidylinositol. The trypanosome also contains a phospholipase C (GPI-PLC) that clea...

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Main Authors:	Webb, Helena, Carnall, Nicola, Vanhamme, Luc, Rolin, Sylvie, Abbeele, Jakke Van Den, Welburn, Sue, Pays, Etienne, Carrington, Mark
Format:	Online
Language:	English
Published:	The Rockefeller University Press 1997
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139819/

id	pubmed-2139819
recordtype	oai_dc
spelling	pubmed-21398192008-05-01 The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice Webb, Helena Carnall, Nicola Vanhamme, Luc Rolin, Sylvie Abbeele, Jakke Van Den Welburn, Sue Pays, Etienne Carrington, Mark Article In the mammalian host, the cell surface of Trypanosoma brucei is protected by a variant surface glycoprotein that is anchored in the plasma membrane through covalent attachment of the COOH terminus to a glycosylphosphatidylinositol. The trypanosome also contains a phospholipase C (GPI-PLC) that cleaves this anchor and could thus potentially enable the trypanosome to shed the surface coat of VSG. Indeed, release of the surface VSG can be observed within a few minutes on lysis of trypanosomes in vitro. To investigate whether the ability to cleave the membrane anchor of the VSG is an essential function of the enzyme in vivo, a GPI-PLC null mutant trypanosome has been generated by targeted gene deletion. The mutant trypanosomes are fully viable; they can go through an entire life cycle and maintain a persistent infection in mice. Thus the GPI-PLC is not an essential activity and is not necessary for antigenic variation. However, mice infected with the mutant trypanosomes have a reduced parasitemia and survive longer than those infected with control trypanosomes. This phenotype is partially alleviated when the null mutant is modified to express low levels of GPI-PLC. The Rockefeller University Press 1997-10-06 /pmc/articles/PMC2139819/ /pubmed/9314532 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Webb, Helena Carnall, Nicola Vanhamme, Luc Rolin, Sylvie Abbeele, Jakke Van Den Welburn, Sue Pays, Etienne Carrington, Mark
spellingShingle	Webb, Helena Carnall, Nicola Vanhamme, Luc Rolin, Sylvie Abbeele, Jakke Van Den Welburn, Sue Pays, Etienne Carrington, Mark The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
author_facet	Webb, Helena Carnall, Nicola Vanhamme, Luc Rolin, Sylvie Abbeele, Jakke Van Den Welburn, Sue Pays, Etienne Carrington, Mark
author_sort	Webb, Helena
title	The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
title_short	The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
title_full	The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
title_fullStr	The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
title_full_unstemmed	The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice
title_sort	gpi-phospholipase c of trypanosoma brucei is nonessential but influences parasitemia in mice
description	In the mammalian host, the cell surface of Trypanosoma brucei is protected by a variant surface glycoprotein that is anchored in the plasma membrane through covalent attachment of the COOH terminus to a glycosylphosphatidylinositol. The trypanosome also contains a phospholipase C (GPI-PLC) that cleaves this anchor and could thus potentially enable the trypanosome to shed the surface coat of VSG. Indeed, release of the surface VSG can be observed within a few minutes on lysis of trypanosomes in vitro. To investigate whether the ability to cleave the membrane anchor of the VSG is an essential function of the enzyme in vivo, a GPI-PLC null mutant trypanosome has been generated by targeted gene deletion. The mutant trypanosomes are fully viable; they can go through an entire life cycle and maintain a persistent infection in mice. Thus the GPI-PLC is not an essential activity and is not necessary for antigenic variation. However, mice infected with the mutant trypanosomes have a reduced parasitemia and survive longer than those infected with control trypanosomes. This phenotype is partially alleviated when the null mutant is modified to express low levels of GPI-PLC.
publisher	The Rockefeller University Press
publishDate	1997
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139819/
_version_	1611421974134784000

The GPI-Phospholipase C of Trypanosoma brucei Is Nonessential But Influences Parasitemia in Mice

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