Microbiol. Rev., Sep 1995, 325-344, Vol 59, No. 3
C Clayton, T Hausler and J Blattner
The kinetoplastid protozoa infect hosts ranging from invertebrates to
plants and mammals, causing diseases of medical and economic importance.
They are the earliest-branching organisms in eucaryotic evolution to have
either mitochondria or peroxisome-like microbodies. Investigation of their
protein trafficking enables us to identify characteristics that have been
conserved throughout eucaryotic evolution and also reveals how far
variations, or alternative mechanisms, are possible. Protein trafficking in
kinetoplastids is in many respects similar to that in higher eucaryotes,
including mammals and yeasts. Differences in signal sequence specificities
exist, however, for all subcellular locations so far examined in detail--
microbodies, mitochondria, and endoplasmic reticulum--with signals being
more degenerate, or shorter, than those of their higher eucaryotic
counterparts. Some components of the normal array of trafficking mechanisms
may be missing in most (if not all) kinetoplastids: examples are
clathrin-coated vesicles, recycling receptors, and mannose
6-phosphate-mediated lysosomal targeting. Other aspects and structures are
unique to the kinetoplastids or are as yet unexplained. Some of these
peculiarities may eventually prove to be weak points that can be used as
targets for chemotherapy; others may turn out to be much more widespread
than currently suspected.
Copyright © 1995, American Society for Microbiology
Protein trafficking in kinetoplastid protozoa
Zentrum fur Molekulare Biologie, Heidelberg, Germany.
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