brucei to hypo-osmolarity or mild alkalinity, which also, strikingly, caused translocation of GPI-PLC from glycosomes (peroxisomes) to the ER.     ///    (c) translocation of GPI-PLC from glycosomes to the ER is important for in vivo cleavage of GPIs.     ///    We examined possible contributions of GPI-PLC to the response of T.     ///    We conclude that: (a) GPI-PLC contributes to loss of GPIs in T.     ///    Glycosome-to-ER movement of GPI-PLC reveals a novel pathway for intracellular protein traffic.     ///    A catalytically inactive Gln81Leu mutant of GPI-PLC failed to cleave GPIs despite being transported from glycosomes to the ER after hypo-osmotic or mild alkaline treatment of the parasites.     ///    (b) access of GPI-PLC to its substrate in vivo can be regulated post-translationally.     ///    (d) Cys347 is part of a peptide motif required for post-translational targeting of GPI-PLC to the ER. 