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Nucleic Acids Research, 2002, Vol. 30, No. 20 4414-4424
© 2002 Oxford University Press

Expression of the human RNA-binding protein HuR in Trypanosoma brucei increases the abundance of mRNAs containing AU-rich regulatory elements

Luis Quijada, Cristina Guerra-Giraldez, Maciej Drozdz, Claudia Hartmann, Henriette Irmer, Claudia Ben-Dov, Marina Cristodero, Martina Ding and Christine Clayton*

ZMBH, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany

*To whom correspondence should be addressed. Tel: +49 6221 546876; Fax: +49 6221 545894; Email: cclayton{at}zmbh.uni-heidelberg.de
Present addresses:
Luis Quijada, Centro de Biología Molecular ‘SO’, Lab CX-203, Universidad Autónoma de Madrid, Cantoblanco, E-28049 Madrid, Spain
Maciej Drozdz, Friedrich Miescher Institute for Biomedical Research, PO Box 2543, 4002 Basel, Switzerland
Henriette Irmer, Yale University School of Medicine, LLCI 8o1, PO Box 208022, 333 Cedar Street, New Haven, CT 06520-8022, USA
Claudia Ben-Dov, INGEBI, Vuelta de Obligado 2490, (1428) Buenos Aires, Argentina
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors

The salivarian trypanosome Trypanosoma brucei infects mammals and is transmitted by tsetse flies. The mammalian ‘bloodstream form’ trypanosome has a variant surface glycoprotein coat and relies on glycolysis while the procyclic form from tsetse flies has EP protein on the surface and has a more developed mitochondrion. We show here that the mRNA for the procyclic-specific cytosolic phosphoglycerate kinase PGKB, like that for EP proteins, contains a regulatory AU-rich element (ARE) that destabilises the mRNA in bloodstream forms. The human HuR protein binds to, and stabilises, mammalian mRNAs containing AREs. Expression of HuR in bloodstream-form trypanosomes resulted in growth arrest and in stabilisation of the EP, PGKB and pyruvate, phosphate dikinase mRNAs, while three bloodstream-specific mRNAs were reduced in abundance. The synthesis and abundance of unregulated mRNAs and proteins were unaffected. Our results suggest that regulation of mRNA stability by AREs arose early in eukaryotic evolution.


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