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

AI Article Synopsis

  • - The nervous system's complexity relies on how individual neurons manage dendritic branching, which is crucial for their structure and function.
  • - The protein KNL-1, typically known for its role in cell division, also regulates dendrite branching in specific neurons by controlling the actin cytoskeleton and preventing excessive growth.
  • - Loss of KNL-1 leads to significant changes in the neuron’s structure, demonstrating its essential role in maintaining proper dendrite architecture and highlighting new insights into nervous system development.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613958PMC
http://dx.doi.org/10.1083/jcb.202311147DOI Listing

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