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A more recent version of this article appeared on September 1, 2004
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Submitted on April 27, 2004
Revised on June 7, 2004
Accepted on June 8, 2004
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*Institute of Cell Biology, University of Bern, CH-3012 Bern, Switzerland; Institute of Zoology, University of Fribourg, CH-1700 Fribourg, Switzerland; Swiss Tropical Institute, CH-4002 Basel, Switzerland
Monitoring Editor: Thomas Fox
In cycling between the mammalian host and the tsetse fly vector, trypanosomes undergo major changes in energy metabolism and surface coat composition. Early procyclic (insect) forms in the tsetse fly midgut are coated by glycoproteins known as EP and GPEET procyclins. EP expression continues in late procyclic forms, while GPEET is down-regulated. In culture, expression of GPEET is modulated by glycerol or glucose. Here we demonstrate that a glycerol-responsive element of 25 nucleotides within the 3' untranslated region of GPEET mRNA also controls expression by glucose and during development in the fly. In trypanosomes, mitochondrial ATP is produced mainly by the acetate:succinate-CoA transferase/succinyl-CoA synthetase (ASCT) cycle, the citric acid cycle and the cytochromes. Silencing of the pyruvate dehydrogenase or succinyl-CoA synthetase from the ASCT cycle by RNA interference induces reexpression of GPEET in late procyclic forms, whereas inhibition of the citric acid cycle or the cytochromes has no effect. In contrast, inhibition of the alternative oxidase, the second branch of the electron transport chain, with salicylhydroxamic acid overrides the effect of glucose or glycerol and causes a reduction in the level of GPEET mRNA. Our results reveal a new mechanism by which expression of a surface glycoprotein is controlled by the activity of mitochondrial enzymes.
Corresponding author. E-mail: erik.vassella{at}izb.unibe.ch
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