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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.
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