Motile cilia of multi-ciliary arrays undulate in a concerted and asymmetric fashion to produce unidirectional fluid flow. Ciliary forces are resisted and translocated to the cell via radially symmetric basal bodies that remain stable in the face of constant ciliary mechanical forces. The Poc1 protein stabilizes such asymmetric forces by organizing and maintaining the radially symmetric triplet microtubules by linking neighboring triplet microtubules. Specific triplet microtubules at the posterior side of the basal body are preferentially lost in poc1Δ basal bodies. This suggests that asymmetric ciliary beating may contribute increased forces on specific triplet microtubules. We find the Poc1 interacting protein, Fop1 to also stabilize basal bodies. Interestingly, Fop1 localizes asymmetrically to the basal body microtubules that preferentially disassemble in poc1Δ and that are predicted to experience high ciliary forces. Finally, Poc1 and Fop1 alter the level of microtubule glutamylation at triplet microtubules, a modification that is predicted to stabilize microtubules. Like Fop1, basal body microtubule glutamylation is asymmetrically localized and, indeed, required for basal body stabilization. However, Poc1, Fop1 and triplet microtubule post-translational modifications appear to act in separate, but redundant, pathways to stabilize basal bodies against asymmetric ciliary forces.