Research uncovers how dynamin regulates PLK-1 during mitosis, indicating its role in spindle assembly and cytokinesis.
Accurate cytokinesis is essential for maintaining genomic integrity. Although the GTPase dynamin has been well studied for its role in vesicular trafficking, its function during mitosis remains poorly understood. In this study, we uncover a novel role for the C. elegans dynamin homolog, DYN-1, in regulating mitotic spindle pole assembly and the spatiotemporal localization of the key mitotic kinase Polo-like kinase 1 (PLK-1). Our studies demonstrate that the depletion of DYN-1 leads to enlarged metaphase spindle poles and elevated levels of centrosome-associated PLK-1. Strikingly, PLK-1 fails to re-localize from centrosomes to the midbody during late mitosis in a subset of DYN-1-depleted embryos, correlating with abnormal PLK-1 localization at the midbody and defective midbody formation. Importantly, this phenotype is likely not due to increased total PLK-1 protein levels, as DNM2 (human homolog of DYN-1) depletion in HeLa cells did not alter total Plk1 abundance. Together, our findings identify DYN-1 as a new regulator of PLK-1 localization during mitosis and suggest that failure to remove PLK-1 from centrosomes may underlie cytokinesis defects that are observed upon DYN-1 depletion.
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Dierlam et al. (2025) studied this question.
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