PT  - JOURNAL ARTICLE
AU  - Yu-Zen Chen
AU  - Vitaly Zimyanin
AU  - Stefanie Redemann
TI  - Mitotic events depend on regulation of PLK-1 levels by the mitochondrial protein SPD-3
AID  - 10.1101/2023.01.11.523633
DP  - 2023 Jan 01
TA  - bioRxiv
PG  - 2023.01.11.523633
4099  - http://biorxiv.org/content/early/2023/01/12/2023.01.11.523633.short
4100  - http://biorxiv.org/content/early/2023/01/12/2023.01.11.523633.full
AB  - 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 StatementThe authors have declared no competing interest.