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Transcriptional regulation of Schistosoma mansoni calreticulin: possible role of AP-1

Published online by Cambridge University Press:  06 April 2009

J. Khalife
Affiliation:
Centre d' Immunologie et de Biologie Parasitaire, INSERM U167, Institut Pasteur, I Rue de Professeur Calmette, B.P. 245, 59019-Lille, France
C. Godin
Affiliation:
Centre d' Immunologie et de Biologie Parasitaire, INSERM U167, Institut Pasteur, I Rue de Professeur Calmette, B.P. 245, 59019-Lille, France
A. Capron
Affiliation:
Centre d' Immunologie et de Biologie Parasitaire, INSERM U167, Institut Pasteur, I Rue de Professeur Calmette, B.P. 245, 59019-Lille, France

Summary

Little is known about the regulation and control of Schistosoma mansoni gene expression. In order to study such mechanisms a gene reporter expression vector construction, under the control of a promoter region derived from the S. mansoni calreticulin gene was used to transfect the human Jurkat T cell line. The promoter region contains potential TATA and CAAT boxes as well as an AP-1 core element. We show here that transcriptional factors of eucaryotic cells may induce a gene reporter activity under the control of a S. mansoni promoter region. Treatment of stably transfected cells with N-acetyl cysteine (NAC), a well-characterized antioxidant which counteracts the effects of reactive oxygen intermediates, enhanced the AP-1 dependent transactivation. This effect was abolished when the SmCaR promoter region was deleted in the AP-1 site. Electrophoretic Mobility Shift Assays showed that the AP-1 sequence of S. mansoni bound to both S. mansoni extracts and in nuclear extracts from Jurkat cells, thus explaining possible activation of AP-1 by NAC. Finally treatment of S. mansoni schistosomula and adult worms with NAC induced an increased synthesis of calreticulin protein suggesting a possible role of redox mechanisms in the regulation of a calreticulin gene transcription process in S. mansoni.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1995

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