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A more recent version of this article appeared on November 1, 2002
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Submitted on February 21, 2002
Revised on July 24, 2002
Accepted on August 5, 2002
1 Institut für Zellbiologie, Universität Bern, Baltzerstrasse 4, CH-3012 Bern, Switzerland (present address: Bernhard Nocht Institut für Tropenmedizin, Abteilung Biochemische Parasitologie, D-20359 Hamburg, Germany)
2 Institut für Zellbiologie, Universität Bern, Baltzerstrasse 4, CH-3012 Bern, Switzerland
* Corresponding author. E-mail address: erik.vassella{at}izb.unibe.ch.
In cycling between the mammalian host and the tsetse fly vector, African trypanosomes undergo adaptive differentiation steps that are coupled to growth control. The signaling pathways underlying these cellular processes are largely unknown. Mitogen-activated protein kinases (MAPKs) are known mediators of growth and differentiation in other eukaryotic organisms. To establish the function of a MAPK homologue, TbMAPK2, in T. brucei, a null mutant was constructed. Bloodstream forms of a 
mapk2/mapk2 clone were able to grow normally and exhibited no detectable phenotype. When these cells were triggered to differentiate in vitro, however, they developed to the procyclic (fly midgut) form with delayed kinetics and subsequently underwent cell cycle arrest. Introduction of an ectopic copy of the TbMAPK2 gene into the null mutant restored its ability to differentiate and to divide. In contrast, a TbMAPK2 mutant, in which the T190 and Y192 residues of the activating phosphorylation site were replaced by A and F, was unable to restore the growth and differentiation phenotypes. Analysis of the DNA content and the nucleus/kinetoplast configuration of individual cells showed that the null mutant was arrested in all phases of the cell cycle and that 25-30% of the cells had failed to segregate their nucleus and kinetoplast correctly. This implies that cell cycle progression by the procyclic form depends on a constitutive stimulus exerted by the signaling cascade operating through TbMAPK2.
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