PROTEIN TRAFFICKING IN KINETOPLASTID PROTOZOA

The kinetoplastid protozoa infect hosts ranging from invertebrates to plants and mammals, causing diseases of medical and economic importanc e. They are the earliest-branching organisms in eucaryotic evolution t o have either mitochondria or peroxisome-like microbodies. Investigati on of their protein trafficking enables us to identify characteristics that have been conserved throughout eucaryotic evolution and also rev eals how far variations, or alternative mechanisms, are possible. Prot ein trafficking in kinetoplastids is in many respects similar to that in higher eucaryotes, including mammals and yeasts. Differences in sig nal sequence specificities exist, however, for all subcellular locatio ns so far examined in detail-microbodies, mitochondria, and endoplasmi c reticulum-with signals being more degenerate, or shorter, than those of their higher eucaryotic counterparts. Some components of the norma l array of trafficking mechanisms may be missing in most (if not all) kinetoplastids: examples are clathrin-coated vesicles, recycling recep tors, and mannose 6-phosphate-mediated lysosomal targeting. Other aspe cts and structures are unique to the kinetoplastids or are as yet unex plained. Some of these peculiarities may eventually prove to be weak p oints that can be used as targets for chemotherapy; others may turn ou t to be much more widespread than currently suspected.