In a study by Charest et al., 2010 a protein signaling complex was discovered and found to regulate the RasC-TORC-PKB/PKBR1 pathway at the leading edge of chemotaxing Dictyostelium discoideum cells. A novel protein, PHR, is a stable member of this Sca1 protein complex. This present study is an in-depth analysis of phr null strains in the regulation of chemotaxis in Dictyostelium cells.

Analyses of phr knockout cells show clear alteration of actin and myosin cytoskeleton dynamics as well as altered cell motility. Though it was discovered that PHR is a stable member of the Sca1 protein signaling complex, it does not affect RasC activity. Intriguingly, phr knockout does seem to modulate the downstream TORC2-mediated phosphorylation of PKB and PKBR1 proteins, despite having no observed effect on RasC activity. Thus, additional roles for PHR in regulating chemotaxis outside of the Sca1 complex was proposed. However, due to the fact that the correct topology of the PHR gene is currently unknown, attempts to generate cells expressing epitope-tagged PHR to test for alternative roles in chemotaxis regulation has proven unsuccessful. The exact functions of PHR in the spatiotemporal regulation of chemotaxis remains unclear.