Multiple pathways for reestablishing PAR polarity in C. elegans embryo

Koch, Laurel A.; Rose, Lesilee S.

doi:10.1016/j.ydbio.2023.05.005

Cited by 4 publications

(1 citation statement)

References 42 publications

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“…PLK-1 is a master regulator in mitosis with multiple important roles to ensure the proper progression through mitosis such as chromosome alignment (Addis Jones et al, 2019), anaphase entry (von Schubert et al, 2015;O'Connor et al, 2015;Jia et al, 2016), and cytokinesis (Burkard et al, 2007;Rezig et al, 2021). In C. elegans PLK-1 was shown to be involved in establishment of polarity (Koch & Rose, 2023), centrosome maturation (Ohta et al, 2021;Nakajo et al, 2022), nuclear lamin disassembly (Velez-Aguilera et al, 2020), and disassembly of the nuclear pore complex (Nkoula et al, 2023). In agreement with the multiple roles of PLK-1, the spd-3(oj35) embryos show a number of defects that could be linked to PLK-1 overexpression.…”

Section: Discussionmentioning

confidence: 99%

Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events

Chen,

Zimyanin,

Redemann

2023

Life Sci. Alliance

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In metazoans, Polo-like kinase (PLK1) controls several mitotic events including nuclear envelope breakdown, centrosome maturation, spindle assembly and progression through mitosis. Here we show that a mutation in the mitochondria-localized protein SPD-3 affects mitotic events by inducing elevated levels of PLK-1 in earlyCaenorhabditis elegansembryos. SPD-3 mutant embryos contain abnormally positioned mitotic chromosomes, show a delay in anaphase onset and asymmetrically disassemble the nuclear lamina. We found that more PLK-1 accumulated on centrosomes, nuclear envelope, nucleoplasm, and chromatin before NEBD, suggesting that PLK-1 overexpression is responsible for some of the observed mitotic phenotypes. In agreement with this, the chromosome positioning defects of thespd-3(oj35)mutant could be rescued by reducing PLK-1 levels. Our data suggests that the mitochondrial SPD-3 protein affects chromosome positioning and nuclear envelope integrity by up-regulating the endogenous levels of PLK-1 during early embryogenesis inC. elegans. This finding suggests a novel link between mitochondria and nuclear envelope dynamics and chromosome positioning by increasing the amount of a key mitotic regulator, PLK-1, providing a novel link between mitochondria and mitosis.

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Section: Discussionmentioning

confidence: 99%

Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events

Chen,

Zimyanin,

Redemann

2023

Life Sci. Alliance

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Cleavage furrow-directed cortical flows bias PAR polarization pathways to link cell polarity to cell division

Ng,

Hirani,

Bland

et al. 2023

Current Biology

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Internal feedback circuits among MEX-5, MEX-6, and PLK-1 maintain faithful patterning in the Caenorhabditis elegans embryo

Vaudano,

Schwager,

Gotta

et al. 2024

Proc. Natl. Acad. Sci. U.S.A.

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Proteins become asymmetrically distributed in the one-cell Caenorhabditis elegans embryo thanks to reaction–diffusion mechanisms that are often entangled in complex feedback loops. Cortical polarity drives the enrichment of the RNA-binding proteins MEX-5 and MEX-6 in the anterior cytoplasm through concentration gradients. MEX-5 and MEX-6 promote the patterning of other cytoplasmic factors, including that of the anteriorly enriched mitotic polo-like kinase PLK-1, but also contribute to proper cortical polarity. The gradient of MEX-5 forms through a differential-diffusion mechanism. How MEX-6 establishes a gradient and how MEX-5 and MEX-6 regulate cortical polarity is not known. Here, we reveal that the two MEX proteins develop concentration asymmetries via similar mechanisms, but despite their strong sequence homology, they differ in terms of how their concentration gradients are regulated. We find that PLK-1 promotes the enrichment of MEX-5 and MEX-6 at the anterior through different circuits: PLK-1 influences the MEX-5 gradient indirectly by regulating cortical polarity while it modulates the formation of the gradient of MEX-6 through its physical interaction with the protein. We thus propose a model in which PLK-1 mediates protein circuitries between MEX-5, MEX-6, and cortical proteins to faithfully establish and maintain polarity.

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Multiple pathways for reestablishing PAR polarity in C. elegans embryo

Cited by 4 publications

References 42 publications

Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events

Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events

Cleavage furrow-directed cortical flows bias PAR polarization pathways to link cell polarity to cell division

Internal feedback circuits among MEX-5, MEX-6, and PLK-1 maintain faithful patterning in the Caenorhabditis elegans embryo

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