Lotmaria passim as an experimental model of trypanosomatid adaptation to the insect gut

Lotmaria passim is a monoxenous trypanosomatid that persistently colonizes the hindgut of the western honey bee, Apis mellifera . Recent chromosome-level genome resources, reverse genetics, conditional protein depletion, omics approaches and experimental infection have shifted research on this parasite from detection surveys towards mechanistic analysis. Here, we synthesize evidence that genome plasticity, flagellar remodeling, Bardet–Biedl syndrome protein complex (BBSome)-dependent membrane organization, ergosterol biosynthesis and extracellular secretion support parasite growth and hindgut colonization. Phenotypes observed in culture do not map simply onto host fitness: deletion of the duplicated LpFCaBP1/LpFCaBP2 genes impairs morphology and motility without significantly reducing infection, whereas disruption of LpBBS2 , LpSC5D1/LpSC5D2 or LpAsp compromises honey bee colonization. These results may suggest that parasite motility is not essential for infection; instead, they highlight membrane homeostasis, protein trafficking, resistance to host clearance, and extracellular functions as additional determinants that should be tested directly. We further propose L. passim as a comparative model for dissecting conserved insect-stage mechanisms shared with other monoxenous trypanosomatids and the insect stages of Leishmania and Trypanosoma . Resolving the signals and molecular machinery controlling haptomonad differentiation, attachment and extracellular community formation will clarify how trypanosomatids adapt to persistent extracellular growth in insect digestive tracts.