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. Author manuscript; available in PMC: 2013 Nov 9.
Published in final edited form as: Annu Rev Microbiol. 2009;63:10.1146/annurev.micro.091208.073353. doi: 10.1146/annurev.micro.091208.073353

Figure 7.

Figure 7

There is a dichotomy in the requirement of the flagellum in procyclic versus bloodstream-form cells. Panels a and b show phenotypes commonly observed in procyclic (PCF) and bloodstream-form (BSF) cells when flagellum proteins are knocked down. (a) Differential interference contrast (DIC) images of uninduced (−Tet) and tetracycline-induced (+Tet) procyclic pfr2 knockdown mutants (PCF Mot −). Induced cells fail in the completion of cytokinesis and accumulate as clusters of distinct cell bodies that remain physically attached at their posterior ends (arrowhead). (b) Phase-contrast images of −Tet and +Tet bloodstream-form trypanin knockdown mutants (BSF Mot −). Induced cells fail in the initiation of cytokinesis and accumulate as amorphous masses with multiple flagella. (c) Schematic representation of the cell cycle and the differing cell cycle blocks in procyclic versus bloodstream flagellum mutants. The cell cycle begins with replication of the basal body and initiation of new flagellum biogenesis. The new flagellum extends along a path defined by the old flagellum, while the basal bodies and associated kinetoplasts (small gray circles) migrate away from each other. In a closed mitotic cycle, the nucleus (large gray circle) is replicated and the new nucleus assumes a position between the new and old kinetoplast/basal body apparatus. Cytokinesis initiates at the tip of the new flagellum (black arrowhead), and cleavage furrow ingression proceeds to the cell posterior, separating the two daughter cells between the new and old flagella. Ultimately, daughter cells are oriented in opposite directions, with their flagella exerting rotational and pulling forces that facilitate final cell separation. Panel a is adapted from Reference 114, panel b from Reference 112, and panel c from Reference 113, with permission.