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Mitotic events depend on regulation of PLK-1 levels by the mitochondrial protein SPD-3

Yu-Zen Chen, View ORCID ProfileVitaly Zimyanin, View ORCID ProfileStefanie Redemann
doi: https://doi.org/10.1101/2023.01.11.523633
Yu-Zen Chen
1Center for Membrane and Cell Physiology, University of Virginia, School of Medicine, Charlottesville, VA, USA
2Department of Molecular Physiology and Biological Physics, University of Virginia, School of Medicine, Charlottesville, VA, USA
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  • For correspondence: yc9jp@virginia.edu
Vitaly Zimyanin
1Center for Membrane and Cell Physiology, University of Virginia, School of Medicine, Charlottesville, VA, USA
2Department of Molecular Physiology and Biological Physics, University of Virginia, School of Medicine, Charlottesville, VA, USA
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Stefanie Redemann
1Center for Membrane and Cell Physiology, University of Virginia, School of Medicine, Charlottesville, VA, USA
2Department of Molecular Physiology and Biological Physics, University of Virginia, School of Medicine, Charlottesville, VA, USA
3Department of Cell Biology, University of Virginia, School of Medicine, Charlottesville, VA, USA
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Abstract

In metazoans, Polo Kinase (Plk1) controls several mitotic events including nuclear envelope breakdown, centrosome maturation and kinetochore assembly. Here we show that mitotic events regulated by Polo Like Kinase (PLK-1) in early C. elegans embryos depend on the mitochondrial-localized protein SPD-3. spd-3 mutant one-cell embryos contain abnormally positioned mitotic chromosomes and prematurely and asymmetrically disassemble the nuclear lamina. Nuclear envelope breakdown (NEBD) in C. elegans requires direct dephosphorylation of lamin by PLK-1. In spd-3 mutants PLK-1 levels are ~6X higher in comparison to control embryos and PLK-1::GFP was highly accumulated at centrosomes, the nuclear envelope, nucleoplasm, and chromosomes prior to NEBD. Partial depletion of plk-1 in spd-3 mutant embryos rescued mitotic chromosome and spindle positioning defects indicating that these phenotypes result from higher PLK-1 levels and thus activity. Our data suggests that the mitochondrial SPD-3 protein controls NEBD and chromosome positioning by regulating the endogenous levels of PLK-1 during early embryogenesis in C. elegans. This finding suggests a novel link between mitochondria and mitotic events by controlling the amount of a key mitotic regulator, PLK-1 and thus may have further implications in the context of cancers or age-related diseases and infertility as it provides a novel link between mitochondria and mitosis.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted January 12, 2023.
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Mitotic events depend on regulation of PLK-1 levels by the mitochondrial protein SPD-3
Yu-Zen Chen, Vitaly Zimyanin, Stefanie Redemann
bioRxiv 2023.01.11.523633; doi: https://doi.org/10.1101/2023.01.11.523633
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Mitotic events depend on regulation of PLK-1 levels by the mitochondrial protein SPD-3
Yu-Zen Chen, Vitaly Zimyanin, Stefanie Redemann
bioRxiv 2023.01.11.523633; doi: https://doi.org/10.1101/2023.01.11.523633

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