Guanine nucleotide exchange factor for arf-6 (By similarity). Involved in response to injury in mechanosensory neurons. Inhibits axon regrowth via microtubule dynamics, possibly by inducing axonal microtubule catastrophes (PubMed:21943602, PubMed:26339988). Limits microtubule growth near the cellular cortex of early embryonic cells (PubMed:21076413). Interacts (via short N-terminal region) with microtubule-associated proteins tac-1 and zyg-8. Present throughout the embryonic cortex during the first embryonic mitosis, but at reduced levels in the posterior cortex (PubMed:21076413). Localizes to the plasma membrane of the soma and processes of neurons. Localizes to the cellular cortex in the steady (uninjured) state. Following injury, transiently relocalizes to the sites marked by the microtubule minus end binding protein ptrn-1 together with tac-1 (PubMed:26339988). Isoform b: Enriched cortically both in the anterior portion of the one-cell zygote and at the blastomere boundary in two-cell embryos. Isoform c: Localizes to nonpolarized cellular cortex in oocytes and early one-cell zygotes and anterior cellular cortex in one-cell embryos subsequent to pseudocleavage. Present at the interface of the AB and P1 cells. Undetectable by the four-cell stage. A short conserved N-terminal region is necessary for the function of this protein (PubMed:21943602, PubMed:26339988). Transient relocalization to microtubule minus ends after neuronal injury also requires this region (PubMed:26339988). Abnormally long and dense microtubules at the cellular cortex of early embryonic cells and growing microtubule plus ends reside at the cortex for up to five times longer. Causes excess centrosome separation and displacement towards the cellular cortex early in mitosis and subsequently a loss of anaphase spindle-pole oscillations and increased rates of spindle elongation. The centrosome separation phenotype is dependent on the motor protein dynein. Weakly delayed nuclear envelope breakdown (PubMed:21076413). Displays mild posterior lateral microtubule (PLM) axon overshooting in development and enhanced PLM regrowth following neuronal injury acting early in regrowth (PubMed:21943602). Axons display elevated numbers of growing microtubules in the steady (uninjured) state and display impenetrant developmental overgrowth in the absence of injury (PubMed:26339988).