Cell-to-flagellum attachment and surface architecture in kinetoplastids.

Lateral attachment of the flagellum to the cell body is mediated by the flagellum attachment zone (FAZ) and defines kinetoplastid cell morphogenesis and pathogenicity. Two interacting proteins, FLA1 and FLA1BP, dominate the attachment in the FAZ extracellular domain and we propose that FLA1 and FLA1BP structure has evolved as a consequence of surface protein coat architecture. The FLA and FLABP gene family have duplicated and expanded in the African trypanosomes, Trypanosoma brucei and Trypanosoma congolense but not in Trypanosoma vivax. A recent T. vivax vaccine candidate generated antibodies that bound to the cell adjacent to the FAZ and we suggest that accessibility to an invariant antigen results from T. vivax expressing only a single FLA1/FLA1BP pair, which needs to maintain flagellum attachment throughout its life cycle across different surface architectures. A key morphological feature of kinetoplastid parasites is the position and length of flagellum attachment to the cell body. This lateral attachment is mediated by the flagellum attachment zone (FAZ), a large complex cytoskeletal structure, which is essential for parasite morphogenesis and pathogenicity. Despite the complexity of the FAZ only two transmembrane proteins, FLA1 and FLA1BP, are known to interact and connect the flagellum to the cell body. Across the different kinetoplastid species, each only has a single FLA/FLABP pair, except in Trypanosoma brucei and Trypanosoma congolense where there has been an expansion of these genes. Here, we focus on the selection pressure behind the evolution of the FLA/FLABP proteins and the likely impact this will have on host–parasite interactions. [ABSTRACT FROM AUTHOR]