Proper development of the nervous system requires directed axonal outgrowth. During early development in C. elegans, the VD GABAergic motor neuron axons are directed anteriorly. Previously, we found that fmi-1/Flamingo, the single C. elegans member of the Celsr-like cadherin superfamily interacts synergistically with Wnt pathway components to regulate anteroposterior (A/P) axonal outgrowth of the VD neurons. In mutant animals, some VD neurons exhibit posterior neurite (PN) outgrowth instead of the stereotypical anterior neurite (AN). In a forward enhancer genetic screen for molecules that demonstrate synergy with the Wnt pathway component, mig-5, to direct A/P outgrowth, we recovered an allele of the cell-adhesion molecule syg-2. To facilitate our genetic analyses, we focused entirely on PNs that occurred in the tail of the animal, where there are normally no GABAergic axons present. In this we found that, individually, loss of function in either mig-5 or syg-2 resulted in a PN in approximately 2% of animals, while 25% of the double mutants had a PN. We found that mutations in the SYG-2 interacting protein, SYG-1, also demonstrated synergy with mig-5 to direct A/P outgrowth, with a similar penetrance in the double mutants. Next we examined interactions between syg-2 and fmi-1. Previously we had reported that 25% of fmi-1;mig-5 mutants exhibited PNs, just like the mig-5;syg-2 mutants. Double mutants of syg-2 and fmi-1 were not synergistic, rather they appeared to be additive (4% penetrance), although, it was also possible that these genes are functioning in a linear pathway. To determine this we examined the triple mutants of fmi-1;mig-5;syg-2, which exhibited PNs in 39% of animals. This suggested that fmi-1 and syg-2 were likely functioning in overlapping pathways, both of which are in parallel to mig-5. Recently however, during analysis of the mig-5;syg-2 doubles we observed PNs emanating from DD6 (in L1 animals). Our previous work showed that the DD neurons were not affected by loss of function in fmi-1. Thus, it is possible the higher penetrance is due to defects present also in DD neurons. We are currently examining the L1 stage animals from the relevant mutant backgrounds to differentiate between these two models. We are also examining where syg-1 and syg-2 are functioning during GABAergic axon development.