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Release of variant surface glycoprot...

Gruszynski, Amy E.

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Release of variant surface glycoprotein during differentiation of Trypanosoma brucei.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Release of variant surface glycoprotein during differentiation of Trypanosoma brucei./
Author:	Gruszynski, Amy E.
Description:	207 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2567.
Contained By:	Dissertation Abstracts International66-05B.
Subject:	Chemistry, Biochemistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3175473
ISBN:	0542139863

Release of variant surface glycoprotein during differentiation of Trypanosoma brucei.
Gruszynski, Amy E.

Release of variant surface glycoprotein during differentiation of Trypanosoma brucei. - 207 p.

Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2567.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2005.

Trypanosoma brucei are digenetic parasites whose lifecycle alternates between the mammalian bloodstream and an insect vector, the tsetse fly. In mammals, replicating long slender parasites transform into non-dividing short stumpy forms. Once in the fly midgut, short stumpy cells differentiate into procyclic forms, a process characterized by the replacement of the bloodstream stage surface coat composed of variant surface glycoprotein (VSG) with a new coat comprised of procyclin. An undefined endoprotease and glycosylphosphatidylinositol-specificphospholipase C (GPI-PLC) have been implicated in releasing the old VSG coat. The role of GPI-hydrolysis has been discounted, however, as GPI-PLC null mutants are fully viable and cytosolic GPI-PLC is topologically sequestered away from extracellular VSG.

ISBN: 0542139863Subjects--Topical Terms:

1017722
Chemistry, Biochemistry.

Release of variant surface glycoprotein during differentiation of Trypanosoma brucei.
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100 1 $a Gruszynski, Amy E. $3 1905105
245 1 0 $a Release of variant surface glycoprotein during differentiation of Trypanosoma brucei.
300 $a 207 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2567.
500 $a Supervisor: James D. Bangs.
502 $a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2005.
520 $a Trypanosoma brucei are digenetic parasites whose lifecycle alternates between the mammalian bloodstream and an insect vector, the tsetse fly. In mammals, replicating long slender parasites transform into non-dividing short stumpy forms. Once in the fly midgut, short stumpy cells differentiate into procyclic forms, a process characterized by the replacement of the bloodstream stage surface coat composed of variant surface glycoprotein (VSG) with a new coat comprised of procyclin. An undefined endoprotease and glycosylphosphatidylinositol-specificphospholipase C (GPI-PLC) have been implicated in releasing the old VSG coat. The role of GPI-hydrolysis has been discounted, however, as GPI-PLC null mutants are fully viable and cytosolic GPI-PLC is topologically sequestered away from extracellular VSG.
520 $a Utilizing a synchronous in vitro differentiation assay with pleomorphic strains, I have reinvestigated these modes of VSG release. GPI-hydrolysis initially mediates release whereas endoproteolysis is upregulated at later time points. GPI-PLC can be physically detected on the surface of intact cells and is apparently primed in the starting short stumpy population. Thus, topology is no longer an issue and GPI-PLC is fully capable of playing a role in VSG release during differentiation. Endoproteolytic release of VSG can be ascribed to a zinc metalloprotease activity. A similar activity is observed when VSG is artificially expressed in procyclic forms. This activity is due to MSP-B, a class of proteases related to Leishmania m&barbelow;ajor s&barbelow;urface p&barbelow;rotease (MSP). Most likely, MSP-B becomes upregulated during differentiation to shed VSG and then remains on the surface of fully transformed procyclics.
520 $a To examine MSP-B and GPI-PLC gene expression, inhibitors of transcription and translation were included in the differentiation assay. Consistent with the hypothesis mentioned above, MSP-B mRNA and protein levels are upregulated at the same time as proteolysis. In contrast, GPI-PLC levels decrease. When transcription or translation is inhibited, VSG release is incomplete and the protein stays substantially cell-associated. Translation inhibition resulted in a marked increase in the mRNA levels of both enzymes, suggesting that labile factors may be involved in their regulation. Overall, the work presented in this thesis helps to provide a better understanding of surface coat remodeling during differentiation of African trypanosomes.
590 $a School code: 0262.
650 4 $a Chemistry, Biochemistry. $3 1017722
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Cell. $3 1017686
690 $a 0487
690 $a 0410
690 $a 0379
710 2 0 $a The University of Wisconsin - Madison. $3 626640
773 0 $t Dissertation Abstracts International $g 66-05B.
790 1 0 $a Bangs, James D., $e advisor
790 $a 0262
791 $a Ph.D.
792 $a 2005
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3175473