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MIG-10 Functions with ABI-1 to Mediate the UNC-6 and SLT-1 Axon Guidance Signaling Pathways

Figure 4

ABI-1 and WVE-1 mediate outgrowth-promoting activity downstream of MIG-10.

(A) Example of normal ALM neuron with a single anterior axon. (B) Example of ALM multipolar defect caused by transgenic expression of MIG-10A by the mec-4::mig-10a transgene. (C) Loss of function mutations abi-1(tm494) and wve-1(ok3308) suppress MIG-10 transgenic expression phenotype. The max-2(nv162) mutation, a likely null, does not suppress the MIG-10 transgenic expression phenotype. The wve-1(ok3308) mutants were maternally rescued. The AVM axon was visualized with a zdIs5 transgene (mec-4::gfp). (D) The abi-1(tm494) loss of function mutation suppresses the AVM multipolar phenotype that results from transgenic expression of MIG-10 in the unc-6; slt-1 double null mutant background. *Statistically significant difference compared to wild-type or unc-6; slt-1 double mutant, z-test for proportions (p<0.005).

Figure 4

doi: https://doi.org/10.1371/journal.pgen.1003054.g004