Abstract
The protozoan parasite Leishmania donovani is part of an early eukaryotic branch and depends on post-transcriptional mechanisms for gene expression regulation. This includes post-transcriptional protein modifications, such as protein phosphorylation. The presence of genes for protein SUMOylation, i.e., the covalent attachment of small ubiquitin-like modifier (SUMO) polypeptides, in the Leishmania genomes prompted us to investigate the importance of the sentrin-specific protease (SENP) and its putative client, SUMO, for the vitality and infectivity of Leishmania donovani. While SENP null mutants are viable with reduced vitality, viable SUMO null mutant lines could not be obtained. SUMO C-terminal processing is disrupted in SENP null mutants, preventing SUMO from covalent attachment to proteins and nuclear translocation. Infectivity in vitro is not affected by the loss of SENP-dependent SUMO processing. We conclude that SENP is required for SUMO processing, but that functions of unprocessed SUMO are critical for Leishmania viability.
Highlights
Leishmania donovani is a protozoan parasite that causes the lethal visceral leishmaniasis, known asKala azar
When screening the L. donovani genome database using BLAST, we identified genes coding for small ubiquitin-like modifier (SUMO) (LdBPK_080480) and SENP (LdBPK_262070)
The SUMO orthologs from the lower eukaryotic clade are distinct from the metazoan
Summary
Leishmania donovani is a protozoan parasite that causes the lethal visceral leishmaniasis, known as. It is a vector-borne pathogen, transmitted by female sandflies of the genus Phlebotomus, in particular. Leishmania exists in two main developmental stages. The parasites are phagocytized by antigen-presenting cells and once inside the phagosomes, convert into ovoid, aflagellated amastigotes as which they may persist in the host for months or years. The leishmaniae differ from their human host and from most other eukaryotes by their lack of gene-specific transcription regulation [1,2,3], relying on modulated RNA stability [4], inducible translation [5] and reversible gene amplification [6,7] instead
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