(De)glutamylation and cell death in Leishmania parasites
Résumé
Trypanosomatids are flagellated protozoan parasites that are very unusual in terms of cyto-skeleton organization but also in terms of cell death. Most of the Trypanosomatid cytoskele-ton consists of microtubules, forming different substructures including a subpellicular corset. Oddly, the actin network appears structurally and functionally different from other eukaryotic actins. And Trypanosomatids have an apoptotic phenotype under cell death conditions, but the pathways involved are devoid of key mammal proteins such as caspases or death receptors, and the triggers involved in apoptotic induction remain unknown. In this article, we have studied the role of the post-translational modifications, deglutamylation and poly-glutamylation, in Leishmania. We have shown that Leishmania apoptosis was linked to poly-glutamylation and hypothesized that the cell survival process autophagy was linked to deglutamylation. A balance seems to be established between polyglutamylation and deglu-tamylation, with imbalance inducing microtubule or other protein modifications characterizing either cell death if polyglutamylation was prioritized, or the cell survival process of autophagy if deglutamylation was prioritized. This emphasizes the role of post-translational modifications in cell biology, inducing cell death or cell survival of infectious agents.
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