Retromer function has been shown to be important for trafficking and localisation of a number of proteins including the CIMPR, sortilin, SorL1, Atg9a and Glut1 (Seaman, 2012; Zavodszky et al., 2014). In cells where retromer function is compromised, Glut1 accumulates in intracellular compartments that are positive for the SNX-BAR protein Snx1, or the lysosomal protein Lamp1 (Steinberg et al., 2013; Zavodszky et al., 2014). It has also been reported that loss of Fam21 function results in Glut1 being mistrafficked from endosomes to the Golgi (Lee et al., 2016). We report here that TBC1D5 knockdown can enhance the membrane association of the retromer CSC and can rescue the reduction in Fam21 recruitment to endosomes in cells expressing the VPS35 D620N mutant. Thus, we wondered whether TBC1D5 knockdown could rescue the trafficking of Glut1 in cells expressing the VPS35 D620N mutant. Cells expressing the VPS35 D620N mutant were treated with siRNA to silence TBC1D5 expression. In Fig. 5A, cells expressing the VPS35 D620N mutant were treated with siRNA to silence TBC1D5 expression. We observed that loss of TBC1D5 appears to reduce the
