Key result
ADF/cofilin gene deletion in Leishmania disrupts cell division, intracellular trafficking, and actin dynamics.
Why the study?
The role of ADF/cofilin in cytokinesis of Leishmania parasites remains largely unknown despite its known importance in flagellum assembly and cell motility.
ADF/cofilin-driven actin dynamics are essential for regulating early events in Leishmania cell division.
Answers are grounded in this paper and cite their sources.
Confirms ADF/cofilin essentiality in Leishmania division; extends actin biology and leaves open therapeutic validation in models.
ADF/cofilin is an actin-dynamics-regulating protein that is required for several actin-based cellular processes such as cell motility and cytokinesis. A homologue of this protein has recently been identified in the protozoan parasite Leishmania, which has been shown to be essentially required in flagellum assembly and cell motility. However, the role of this protein in cytokinesis remains largely unknown. We show here that deletion of the gene encoding ADF/cofilin in these organisms results in several aberrations in the process of cell division. These aberrations include delay in basal body and kinetoplast separation, cleavage furrow progression and flagellar pocket division. In addition to these changes, the intracellular trafficking and actin dynamics are also adversely affected. All these abnormalities are, however, reversed by episomal complementation. Together, these results indicate that actin dynamics regulates early events in Leishmania cell division.
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Tammana et al. (2010) studied Leishmania infection / parasite biology. Deletion of the gene encoding ADF/cofilin vs. Episomal complementation was evaluated on Aberrations in the process of cell division (basal body and kinetoplast separation, cleavage furrow progression, flagellar pocket division). Deletion of the ADF/cofilin gene in Leishmania causes aberrations in cell division, intracellular trafficking, and actin dynamics, which are reversed by episomal complementation.
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