The minus-ends of microtubules have been implicated as part of a damage sensor to initiate remodeling of nerve cells.

The protein PTRN-1 anchors microtubules in neuronal branches to promote proper neuron morphology and function in Caenorhabditis elegans.

The C. elegans ninein homolog NOCA-1 is important for the assembly of non-centrosomal microtubule arrays required for embryo production, nuclear positioning and larval development.

Genetic, developmental and pharmacological analysis in Caenorhabditis elegans demonstrate that ATAT-2 tubulin acetyltransferase activity regulates synapse maintenance by acting within the RPM-1 signaling network, but independent of the DLK-1 MAP3K.

Genetic suppressor screens with C. elegans reveal a novel function for the Death Associated Protein Kinase in regulation of epithelial microtubule dynamics.

Severing axons in C. elegans reveals a mechanism by which the axons sense acute damage and respond by sequential remodeling of their microtubule cytoskeleton.

PAR-6 and PKC-3/aPKC are essential for postembryonic development of C. elegans and control the organization of non-centrosomal microtubule bundles in the epidermis, likely through recruitment of NOCA-1/Ninein.

A minus-end-binding stabilizes minus-end-out microtubules in dendrites, which are required for dendrite-specific pruning during neuronal remodelling.

During intestinal development, apical PAR complex proteins keep apical domains and junctions continuous between cells as they divide and elongate, and ultimately build a continuous functional tube.

Microtubules orchestrate wound repair and innate immune response in the Caenorhabditis elegans epidermis.