Kinesins in Caenorhabditis elegans neuronal morphogenesis

TL;DR

This review explores how kinesins in C. elegans contribute to the development of neurons by regulating transport and the cytoskeleton.

Contribution

The paper provides a comprehensive overview of kinesin functions in C. elegans neuronal morphogenesis, emphasizing their roles in transport and cytoskeletal regulation.

Findings

Kinesins in C. elegans are essential for neuronal morphogenesis through intracellular transport and cytoskeletal regulation.

Genetic screens in C. elegans have identified various kinesin mutants, including gain-of-function and temperature-sensitive mutants.

CRISPR/Cas9 genome editing has enabled precise genetic analysis of kinesins in C. elegans.

Abstract

Neuronal morphogenesis is regulated by intracellular transport and cytoskeletal dynamics. Kinesin superfamily proteins (KIFs), or kinesins, function as molecular motors for intracellular transport and as regulators of the microtubule cytoskeleton, making them essential for neuronal development. Caenorhabditis elegans has been widely used as a model organism to study neuronal morphogenesis. Due to the critical roles of kinesins in neuronal functions, numerous kinesin mutants, including unique gain-of-function mutants and temperature-sensitive mutants, have been identified through forward genetic screens in C. elegans. The availability of whole-genome knockout resources and CRISPR/Cas9 genome editing has further enabled precise genetic analysis, facilitating the modelling of human kinesin-related diseases in C. elegans. In this review, we discuss the functions of C. elegans kinesins in neuronal morphogenesis, focusing on their roles in neuronal transport and cytoskeletal regulations.

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