Here we describe the non-canonical control of gene expression in Leishmania , a single-cell parasite that is responsible for one of the major neglected tropical diseases. We discuss the lack of regulated RNA synthesis, the post-transcriptional gene regulation including RNA stability and regulated translation. We also show that genetic adaptations such as mosaic aneuploidy, gene copy number variations and DNA sequence polymorphisms are important means for overcoming drug challenge and environmental diversity. These mechanisms are discussed in the context of the unique flow of genetic information found in Leishmania and related protists.

A key factor in the successful infection of a mammalian host by Leishmania parasites is their conversion from extracellular motile promastigotes into intracellular amastigotes. We discuss the physical and chemical triggers that induce this conversion and the accompanying changes at the molecular level crucial for the survival of these intracellular parasites. Special emphasis is given to the reliance of these trypanosomatids on the post-transcriptional regulation of gene expression but also to the role played by protein kinases, chaperone proteins and proteolytic enzymes. Lastly, we offer a model to integrate the transduction of different stress signals for the induction of stage conversion.

Leishmania parasites are important pathogens with a global impact and cause poverty-related illness and death. They are devoid of classic cis - and trans -acting transcription regulators but use regulated translation and gene copy number variations to adapt to hosts and environments.

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