Authors

Discussion

The Trypanosoma (T) brucei life cyclealternates between the tsetse fly vector and the mammalian host. In the insect, T. brucei undergoes several developmental stages until it reaches the salivary gland and differentiates into the metacyclic form (MCF), which is capable of infecting mammals. Mammalian infectivity is dependent on expression of the metacyclic variant surface glycoprotein (mVSG) genes in the mature metacyclic. Recently, VEX complex proteins had been identified as essential for monoallelic VSG expression in T. brucei bloodstream form, however, monoallelic expression during metacyclic differentiation is poorly understood. To better understand the transition to mature metacyclics and the control of mVSG expression we are studying the role of the VEX complex in this process.  We show that modulating VEX1 expression leads to a dysregulation of monoallelic mVSG expression during MCF differentiation. Additionally, following both in vivo and in vitro metacyclic differentiation, we observed a relocation of VEX1, suggesting a role for VEX1 in mVSG expression. Additionally, preliminary results show that constitutive over-expression of VEX1 in the pleomorphic Antat1.1 cell line, promotes colonization of the tsetse fly salivary gland. This suggest a role for the VEX complex in the metacyclic differentiation process and their capacity to become infectious to the mammalian host.