Abstract
ABSTRACTCentrosomes are the primary microtubule-organizing centers that orchestrate microtubule dynamics during the cell cycle. The correct number of centrosomes is pivotal for establishing bipolar mitotic spindles that ensure accurate segregation of chromosomes. Thus, centrioles must duplicate once per cell cycle, one daughter per mother centriole, the process of which requires highly coordinated actions among core factors and modulators. Protein phosphorylation is shown to regulate the stability, localization and activity of centrosome proteins. Here, we report the function of Casein kinase II (CK2) in early Caenorhabditis elegans embryos. The catalytic subunit (KIN-3/CK2α) of CK2 localizes to nuclei, centrosomes and midbodies. Inactivating CK2 leads to cell division defects, including chromosome missegregation, cytokinesis failure and aberrant centrosome behavior. Furthermore, depletion or inhibiting kinase activity of CK2 results in elevated ZYG-1 levels at centrosomes, restoring centrosome duplication and embryonic viability to zyg-1 mutants. Our data suggest that CK2 functions in cell division and negatively regulates centrosome duplication in a kinase-dependent manner.
Highlights
Control of proper centrosome number is crucial for the fidelity of cell division (Gönczy, 2015)
Our results suggest that the protein kinase Casein kinase 2 holoenzyme (CK2) holoenzyme physically associates with SZY-20 in vivo
C. elegans protein kinase CK2 functions in cell division during embryogenesis In this study, we have investigated the function of the holoenzyme CK2 in early C. elegans embryos
Summary
Control of proper centrosome number is crucial for the fidelity of cell division (Gönczy, 2015). Centrosomes organize microtubules to direct the formation of bipolar mitotic spindles that contribute to accurate segregation of genomic content. Centrosomes comprise two orthogonally arranged centrioles surrounded by a dense network of proteins termed pericentriolar material (PCM). Centrioles must duplicate exactly once per cell cycle to provide daughter cells with the correct number of centrosomes. Cells with abnormal centrosome number are prone to errors in DNA segregation and cytokinesis, leading to genomic instability and tumorigenesis (Godinho and Pellman, 2014). Genetic analyses in C. elegans have elucidated a core set of five conserved factors required for centriole duplication, including the Plk4-related kinase ZYG-1 (O’Connell et al, 2001), the coiled coil
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