GO:0060285 cilium-dependent cell motility

Cilium-dependent cell motility (GO:0060285) is a biological process in which a cell moves because of the motion of one or more eukaryotic cilia. Eukaryotic cilia are microtubule-based organelles that extend from the cell surface and are anchored at a basal body, and their coordinated beating or signaling can drive cell movement or guide migration. This term is distinct from actin-based motility and encompasses both motile cilia and primary cilia that influence movement through signaling. Understanding this process is important because ciliary motility is essential for development, reproduction, and neuronal positioning, and its dysfunction contributes to a range of human disorders [1,3,4]. Researchers study GO:0060285 to identify the genes, structural components, and signaling pathways that control ciliary motion and to model ciliopathies and related diseases [1,3,4]. Recent work has shown that primary cilium-dependent cAMP/PKA signaling at the centrosome regulates neuronal migration, directly linking ciliary signaling to cell motility. In addition, CDKL kinase regulates the length of the ciliary proximal segment, a structural feature that influences cilium function and motility. Pathogenic LRRK2 mutations cause loss of primary cilia and Neurturin in striatal parvalbumin interneurons, connecting ciliary dysfunction to neurodegeneration. Proteomic analysis of spermatozoa in domesticated pigeons has identified proteins that may support flagellar motility, providing candidates for further study.

GO:0060285 cilium-dependent cell motility is defined as cell motility due to the motion of one or more eukaryotic cilia. A eukaryotic cilium is a specialized organelle consisting of a filiform extrusion of the cell surface, bounded by an extrusion of the cytoplasmic (plasma) membrane, and containing a regular longitudinal array of microtubules anchored basally in a centriole. In practice, this means that the cell's movement is powered or guided by ciliary beating or by ciliary signaling that regulates the motility machinery.

Cilium-dependent cell motility is important because cilia are ancient, conserved organelles that coordinate cell movement during development, tissue repair, and reproduction, and because defects in ciliary structure or signaling underlie a broad spectrum of human diseases [1,3,4]. Studying this process helps researchers understand how cells sense and respond to their environment, how signaling molecules such as cAMP/PKA are organized at the centrosome, and how mutations in ciliary genes lead to neurodegeneration and other disorders [1,4].

The following genes and proteins have been experimentally linked to cilium-dependent cell motility or its regulation in the cited literature.

Cilium-dependent cell motility is regulated at multiple levels. CDKL kinase controls the length of the ciliary proximal segment, which influences cilium function and motility. Primary cilium-dependent cAMP/PKA signaling at the centrosome regulates neuronal migration, showing that second-messenger signaling is a key regulatory input. Pathogenic LRRK2 mutations cause loss of primary cilia and Neurturin in striatal parvalbumin interneurons, indicating that LRRK2 activity is required for ciliary maintenance. Proteomic identification of spermatozoa proteins suggests that flagellar motility is supported by a defined set of structural and regulatory proteins.

Pathogenic LRRK2 mutations cause loss of primary cilia and Neurturin in striatal parvalbumin interneurons, linking cilium-dependent processes to neurodegeneration. This suggests that ciliary dysfunction may contribute to Parkinson's disease-related pathology.

Primary cilium-dependent cAMP/PKA signaling at the centrosome regulates neuronal migration, so disruption of this pathway can impair brain development. Defects in ciliary signaling may lead to migration disorders.

CDKL kinase regulates the length of the ciliary proximal segment, and its dysfunction could contribute to ciliopathies characterized by abnormal cilia. Structural ciliary defects often impair motility and signaling.

Proteomic analysis of spermatozoa in domesticated pigeons identifies proteins required for flagellar motility, which may be relevant to male fertility disorders. Defects in these proteins could impair cilium-dependent motility.

Proteomic analysis of spermatozoa in domesticated pigeons has been used to identify proteins involved in flagellar motility. This approach provides a catalog of candidate effectors for cilium-dependent cell motility.

Imaging of primary cilium-dependent cAMP/PKA signaling at the centrosome has been used to study neuronal migration. Live imaging allows researchers to track ciliary motion and its effects on cell movement.

Studies of CDKL kinase have used genetic perturbation to show that it regulates the length of the ciliary proximal segment. Such experiments link structural changes to cilium function.

Pathogenic LRRK2 mutations have been modeled to demonstrate loss of primary cilia and Neurturin in striatal parvalbumin interneurons. This method connects ciliary dysfunction to neurodegeneration.

Researchers studying cilium-dependent cell motility-related genes often need to determine whether a candidate gene is causally involved in ciliary motion, signaling, or disease. EDITGENE provides CRISPR-based models and screening services to accelerate this work.

GO:0060285 cilium-dependent cell motility is a fundamental biological process in which eukaryotic cilia drive or guide cell movement through mechanical beating and signaling. Key regulators such as CDKL and LRRK2 control ciliary structure and maintenance, and their dysfunction is linked to neurodegeneration and other disorders [3,4]. Continued research using proteomics, imaging, and CRISPR models will clarify how ciliary proteins and signaling pathways coordinate motility in health and disease [1,2,3,4].