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The kinetochore protein KNL-1 regulates the actin cytoskeleton to control dendrite branching

2024/11/15 by Henrique Alves Domingos, Mattie Green, Vasileios R. Ouzounidis +3 · 1 voice
Biochemistry, Genetics and Molecular Biology · #Genetics, Aging, and Longevity in Model Organisms #Microtubule and mitosis dynamics #Photosynthetic Processes and Mechanisms

paper · pdf · doi:10.1083/jcb.202311147

openalex publication_date 2024/11/15 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/02

Abstract

The function of the nervous system is intimately tied to its complex and highly interconnected 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 Caenorhabditis 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 postmitotic 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.

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