Postnatal mice containing a null mutation in the SNX27 gene exhibit severe developmental defects and die before weaning (Cai et al., 2011), indicating that SNX27 is involved in multiple signaling pathways in the mouse. Indeed, SNX27 is expressed in a variety of cell types, including brain, heart, kidney and lung (Kajii et al., 2003). To avoid lethality, we created a conditional knockout of SNX27 in mice that targeted only DA neurons (Figure 1A – see Methods for details). This was accomplished by crossing a pre-conditional floxed Snx27 line (Snx27fl/fl) with a DAT-Cre+/− line, where Cre recombinase expression is under the control of the dopamine transporter gene (DAT or Slc6j) (Zhuang et al., 2005) (Figure 1A). As expected, immunostaining for SNX27 protein revealed a loss of SNX27 protein expression in midbrain TH-positive neurons of DAT-Cre+/− × Snx27fl/fl mice, which we refer to as SNX27DA KO mice (Figure 1A–C). Importantly, SNX27DA KO mice were viable, bred normally and lived into adulthood. Moreover, the number of TH positive neurons in the VTA/SN did not appear to differ from control mice (Figure 1D). We
