HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 281, Issue 29, 20068-20076, July 21, 2006

This Article Full Text Full Text (PDF) All Versions of this Article: 281/29/20068    most recent M603265200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rodríguez-Contreras, D. Articles by Landfear, S. M. Search for Related Content PubMed PubMed Citation Articles by Rodríguez-Contreras, D. Articles by Landfear, S. M. Social Bookmarking                      What's this?

Metabolic Changes in Glucose Transporter-deficient Leishmania mexicana and Parasite Virulence^*

From the Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon 97239

Leishmania mexicana are parasitic protozoa that express a variety of glycoconjugates that play important roles in their biology as well as the storage carbohydrate -mannan, which is an essential virulence factor for survival of intracellular amastigote forms in the mammalian host. Glucose transporter null mutants, which are viable as insect form promastigotes but not as amastigotes, do not take up glucose and other hexoses but are still able to synthesize these glycoconjugates and -mannan, although at reduced levels. Synthesis of these carbohydrate-containing macromolecules could be accounted for by incorporation of non-carbohydrate precursors into carbohydrates by gluconeogenesis. However, the significantly reduced level of the virulence factor -mannan in the glucose transporter null mutants compared with wild-type parasites may contribute to the non-viability of these null mutants in the disease-causing amastigote stage of the life cycle.

Received for publication, April 5, 2006 , and in revised form, May 11, 2006.

^* This work was supported by Grant AI25920 from the National Institutes of Health (to S. M. L.) and a post-doctoral fellowship from the American Heart Association (to D. R.-C.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Molecular Microbiology and Immunology, Oregon Health & Science University, 3181 S.W. Sam Jackson Park Rd., Portland, OR 97239. Tel.: 503-494-2624; Fax: 503-494-6862; E-mail: landfear{at}ohsu.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?