High-speed holographic microscopy shows that Leishmania parasites modify their swimming behaviour to target human macrophages.

Duplication of Leishmania chromosomes combines S-phase DNA replication initiated at a single internal region with subtelomeric DNA replication detectable outside S-phase, potentially explaining genome plasticity in this important parasite.

Genomic data for the parasites that cause visceral leishmaniasis provides the first global picture of the diversity and evolution of the pathogen and the epidemiology of this fatal tropical disease.

The X-ray structure of the SAS-6 cartwheel hub from Leishmania major demonstrates that SAS-6 can be sufficient to determine centriolar cartwheel symmetry.

LeishBASEedit enables gene editing in Leishmania without requiring DNA double-strand breaks, homologous recombination, or donor DNA, thereby facilitating loss-of-function screens via delivery of plasmid libraries and regardless of limitations due to gene copy number variations and/or lack of RNAi components.

Following exposure of Leishmania culture promastigotes to DNA stress, single-cell RNA sequencing reveals discrete clusters of cells associated with efficient generation of hybrids between different species and strains in vitro marked by expression of the ancestral gamete fusogen HAP2.

Genome sequencing reveals the evolution and epidemiology of Leishmania donovani in the Indian subcontinent, where epidemics have caused up to 30,000 deaths per year.

Biological and pharmacokinetic studies indicate that the anti-tubercular drug, delamanid, could be repurposed for the treatment of visceral leishmaniasis.

Using advanced volume electron microscopy, the ultrastructural and spatial organisation of Leishmania parasites strongly adhered to the gut of its sand fly vector was defined.

Basalins are intrinsically disordered proteins with astonishingly high-sequence divergence that are essential for building the transition zone basal plate and for proper central pair nucleation.