Fig. 6. Model of Semaphorin 1 and Plexin 1 signaling in male ray 1 positioning. (A) In a wild-type genetic background, we find that MIG-2 and CED-10 (RAC GTPAses) are probably redundant in preventing anterior displacement of ray 1 cells (however, see Discussion). There is a requirement for UNC-73 (RAC GEF) in MIG-2 and CED-10 function. Some UNC-73 functions are required in parallel with PLX-1 for preventing this phenotype. RHO-1 GTPases, and the RHO-kinases LET-502 and K08B12.5, appear to be required in parallel with the PLX-1 and UNC-73/MIG-2/CED-10 pathways to prevent anterior ray 1 displacement, but the analyses do not rule out a possible direct feed-forward from PLX-1 signaling to RHO-family GTPase signaling (dashed arrow on left). Debilitation of UNC-73, MIG-2 and CED-10 displaces ray 1 anterior to normal, whereas debilitation of UNC-33 prevents anterior ray 1 displacement. At high (normal) levels of MIG-2 and CED-10, SMP-1 and SMP-2 signaling through PLX-1 helps to prevent anterior displacements of ray 1 (pathway in blue). However, a conversion of PLX-1 function occurs at low levels of both MIG-2 and CED-10 [genotype mig-2(mu28); ced-10(n1993)/+], as a stimulation of the ray 1 anterior positioning function occurs (pathway in red). This implies that high (normal) levels of RAC GTPases (MIG-2 and CED-10) prevent the switch in the polarity of PLX-1 output. Ray anterior displacements require CRMP/UNC-33, which could act as an effector of PLX-1 at low RAC levels (dashed arrow on right), or could act independently. (B) A cell migration model for positioning of ray 1 cells during male development. In a wild-type background [normal mig-2(+) and ced-10(+) (rac) levels], expression of Semaphorin 1 proteins from the hook primordium (green) attracts PLX-1-expressing ray 1 cells (purple) toward the posterior side. At low mig-2(+) and ced-10(+) (rac) levels [genotype mig-2(mu28); ced-10(n1993)/+], ray 1 cells are repulsed away from sources of Semaphorin 1 proteins.