The microtubule cytoskeleton is spatially reorganized from the centrosomes to new subcellular sites during cell differentiation, a process accomplished by a reassignment of microtubule organizing center (MTOC) proteins and function. In the developing C. elegans intestine, all MTOC function is reassigned from the centrosomes to the future apical cell membrane during cell polarization; microtubules grow from and are anchored at the apical membrane. This MTOC reassignment occurs relatively rapidly and synchronously in all polarizing intestinal cells and so affords us a system in which to probe the mechanisms controlling the formation of these new non-centrosomal MTOCs at the onset of cell differentiation. We find that microtubule minus-end binding proteins NOCA-1, PTRN-1, Ninein-like protein (T04F8.6), and γ-tubulin small complex (γ-TuSC) proteins GIP-1/GCP3, GIP-2/GCP2, and TBG-1/γ-tubulin localize to the apical MTOC. To determine the requirement of these proteins in membrane MTOC formation, we are taking advantage of a tissue-specific protein degradation system (Armenti et al. 2014) to deplete endogenous GIP-1 exclusively in the developing intestine around the time of MTOC reassignment. Using this method, we have found that GIP-1 is not required for the apical localization of the apical polarity protein PAR-3; however, GIP-1 is required for normal apical localization of GIP-2 and TBG-1. Surprisingly, apical microtubules are present in GIP-1-depleted embryos, suggesting an alternative method for nucleation and/or localization of microtubules at these sites. In other tissues, it has previously been reported that ptrn-1 functions in parallel to γ-TuSC to generate non-centrosomal microtubules; however, we find apically localized microtubules after depletion of both GIP-1 and PTRN-1 in developing intestines, suggesting the existence of a third pathway. GIP-1 appears to be essential for normal mitosis in the developing intestine as has been reported in the early embryo; embryos depleted of intestinal GIP-1 have fewer intestinal nuclei as compared to control embryos, and these nuclei appear consistently enlarged. Together, these results demonstrate that apical GIP-1 localization is required for the polarization of γ-TuSCs in the developing intestine, but that additional pathways exist to establish an apical MTOC. Furthermore, centrosomal GIP-1 localization is required for normal spindle formation and mitosis. Further investigation is necessary to determine how γ-TuSC-independent microtubules are generated at the apical membrane, and whether this population of microtubules differs from those of control embryos in quantity and dynamics.