ABSTRACT
Precise control of dendrite branching is essential for the formation of neural circuits, yet the mechanisms that regulate this process remain poorly understood. Here we show that the kinetochore protein KNL-1, known for its role in chromosome-microtubule coupling during mitosis, together with its binding partners, the KMN network, regulate dendritic branching in the C. elegans mechanosensory neuron, PVD, in a cell division independent manner. Neuron-specific degradation of KNL-1 results in excess dendrite branching and fusion events, predisposes PVD to age-dependent degeneration, and impairs animal sensory behavior. Surprisingly, these effects are not attributable to mis-regulation of the microtubule cytoskeleton. Instead, KNL-1 degradation alters the dynamics of F-actin, an established driver of dendrite branching. Epistasis analysis shows that KNL-1 counters the activity of the RacGEF TIAM-1, a downstream effector of dendrite guidance receptors. These findings establish that the microtubule coupling KMN network promotes dendrite branching by regulating the actin cytoskeleton and provide insight into how the cytoskeleton shapes dendritic architecture.
Competing Interest Statement
The authors have declared no competing interest.