The Kinetochore Protein KNL-1 Regulates Actin Cytoskeleton Dynamics to Promote Dendrite Branching in Sensory Neurons
The function of the nervous system is intimately tied to its complex and highly inter-connected architecture. Precise control of dendritic branching in individual neurons is central to building the complex structure of the nervous system. Here we show that the kinetochore protein KNL-1 and its associated KMN (Knl1/Mis12/Ndc80 complex) network partners, typically known for their role in chromosome-microtubule coupling during mitosis, control dendrite branching in the C. elegans mechanosensory PVD neuron. KNL-1 restrains excess dendritic branching and promotes contact-dependent repulsion events, ensuring robust sensory behavior and preventing premature neurodegeneration. Unexpectedly, KNL-1 loss resulted in significant alterations of the actin cytoskeleton alongside changes in microtubule dynamics within dendrites. We show that KNL-1 modulates F-actin dynamics to generate proper dendrite architecture, and that its N-terminus can initiate F-actin assembly. These findings reveal that the post-mitotic neuronal KMN network acts to shape the developing nervous system by regulating the actin cytoskeleton and provide new insight into the mechanisms controlling dendrite architecture.