Figure 7.

Models for enhancement of Gα₁₃-evoked neurite retraction by R7-RGS heterotrimers. R7-RGS heterotrimers form macromolecular complexes with G₁₃ heterotrimers and remain bound to Gα₁₃ upon activation of the G protein. Activated Gα₁₃ recruits a RhoGEF to the plasma membrane where it activates RhoA and downstream signaling events that ultimately result in neurite retraction. RhoGEFs also negatively regulate this process because they are GAPs for Gα₁₃. R7-RGS heterotrimers could facilitate Gα₁₃-evoked neurite retraction by two non-mutually exclusive mechanisms: 1) enhancing recruitment and activation of RhoGEFs, thereby enhancing RhoA signaling, or 2) inhibiting RhoGEF GAP activity for Gα₁₃, thereby prolonging Gα₁₃ activity.