Skip to main content
. Author manuscript; available in PMC: 2021 Nov 22.
Published in final edited form as: Neuron. 2019 Mar 19;102(3):602–620.e9. doi: 10.1016/j.neuron.2019.02.034

Figure 8. Model for Temporal and Context-Dependent Control of Motor Axon Guidance by p190.

Figure 8.

(A) (Left) p190 suppresses Netrin-1/DCC attractive signaling in a GAP-independent manner and collaborates with Cxcl12/Cxcr4 pathway to control motor axon exiting from the spinal cord. Netrin-1 deposited on the pial surface of the spinal cord is a substrate for dorsal commissural neurons (dCN) that project to the midline but must be ignored by motor axons that select ventral exit points in response to Cxcl12/Cxcr4 chemoattraction. (Right) DCC attractive signaling is turned-on in p190 mutants, causing inappropriate motor axon attraction to pial-associated Netrin-1 that results in intra-spinal axon growth. Cxcr4 is unable to compensate for derepression of DCC signaling. (B) (Left) In the periphery, motor axon targeting to limb muscles depends on suppression of Rho signaling by p190-GAP activity. DCC signaling is switched on enabling axons to respond to target-derived Netrin-1 (Poliak et al., 2015). (Right) Rho signaling is abnormally enhanced in the absence of p190, causing mistargeting of motor neurons that innervate the dorsal limb muscles (LMCL). Motor axons that innervate ventral muscles (LMCM) are unaffected.