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Cold shock and regulation of surface protein trafficking convey sensitization
 

Summary: Cold shock and regulation of surface
protein trafficking convey sensitization
to inducers of stage differentiation
in Trypanosoma brucei
Markus Engstler1
and Michael Boshart2
Ludwig-Maximilians-Universität, Department Biologie I, Genetik, 80638 München, Germany
Transmission of a protozoan parasite from a vertebrate to invertebrate host is accompanied by cellular
differentiation. The signals from the environment that trigger the process are poorly understood. The model
parasite Trypanosoma brucei proliferates in the mammalian bloodstream and in the tsetse fly. On ingestion
by the tsetse, the trypanosome undergoes a rapid differentiation that is marked by replacement of the variant
surface glycoprotein (VSG) coat with GPI-anchored EP and GPEET procyclins. Here we show that a cold shock
of T > 15°C is sufficient to reversibly induce high-level expression of the insect stage-specific EP gene in the
mammalian bloodstream stages of T. brucei. The 3 -UTR of the EP mRNA is necessary and sufficient for the
increased expression. During cold shock, EP protein accumulates in the endosomal compartment in the
proliferating, slender, bloodstream stage, whereas the EP is present on the plasma membrane in the quiescent,
stumpy, bloodstream stage. Thus, there is a novel developmentally regulated cell surface access control
mechanism for a GPI-anchored protein. In addition to inducing EP expression, cold shock results in the
acquisition of sensitivity to micromolar concentrations of cis-aconitate and citrate by stumpy but not slender
bloodstream forms. The cis-aconitate and citrate commit stumpy bloodstream cells to differentiation to the

  

Source: Arnold, Jonathan - Nanoscale Science and Engineering Center & Department of Genetics, University of Georgia

 

Collections: Biotechnology