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Peer-reviewedCC BY 4.0PLOS One

Divergence of cortical force-generating mechanisms underlies differences in spindle behavior between C. elegans and C. inopinata

  • Shun Oomura1
  • Koji Kyoda2
  • Shuichi Onami2
  • Nami Haruta1
  • Asako Sugimoto1
  1. 1Laboratory of Developmental Dynamics, Graduate School of Life Sciences, Tohoku University, Sendai, Japan
  2. 2Laboratory for Developmental Dynamics, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan
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Abstract

Microtubule-dependent pronuclear migration and mitotic spindle positioning are fundamental processes during the first embryonic division in many animals. In the one-cell embryo of Caenorhabditis elegans, these events are regulated by well-characterized pulling forces acting on astral microtubules, including cortical forces mediated by the Gα-GPR-LIN-5 dynein complex. Although the overall framework of these dynamics is conserved, recent studies have revealed substantial interspecies variation in their regulation. Here, we investigated nuclei and mitotic spindle behaviors in one-cell embryos of Caenorhabditis inopinata, the closest known relative of C. elegans, using live-cell imaging and functional perturbation. We found that C. inopinata embryos exhibit altered pronuclear migration, reduced anaphase spindle oscillations, and slower centrosome diffusion during telophase compared with C. elegans. These differences suggest weaker cortical pulling forces. Functional analyses using RNA interference showed that GPR retains its essential role in force generation, whereas the contribution of the microtubule depolymerizing kinesin KLP-7 is reduced in C. inopinata. Our results point to evolutionary changes in microtubule-regulated spindle dynamics, and provide insight into how conserved cellular processes can diversify through subtle changes in their underlying mechanisms.

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Cite

BibTeXRIS
BibTeX
@article{oomura2026divergence,
  title = {{Divergence of cortical force-generating mechanisms underlies differences in spindle behavior between C. elegans and C. inopinata}},
  author = {Shun Oomura and Koji Kyoda and Shuichi Onami and Nami Haruta and Asako Sugimoto},
  journal = {PLOS One},
  year = {2026},
  month = oct,
  doi = {10.1371/journal.pone.0352057},
  url = {https://doi.org/10.1371/journal.pone.0352057},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Divergence of cortical force-generating mechanisms underlies differences in spindle behavior between C. elegans and C. inopinata
AU  - Shun Oomura
AU  - Koji Kyoda
AU  - Shuichi Onami
AU  - Nami Haruta
AU  - Asako Sugimoto
PY  - 2026
DA  - 2026/10/27
JO  - PLOS One
DO  - 10.1371/journal.pone.0352057
UR  - https://doi.org/10.1371/journal.pone.0352057
AB  - Microtubule-dependent pronuclear migration and mitotic spindle positioning are fundamental processes during the first embryonic division in many animals. In the one-cell embryo of Caenorhabditis elegans, these events are regulated by well-characterized pulling forces acting on astral microtubules, including cortical forces mediated by the Gα-GPR-LIN-5 dynein complex. Although the overall framework of these dynamics is conserved, recent studies have revealed substantial interspecies variation in their regulation. Here, we investigated nuclei and mitotic spindle behaviors in one-cell embryos of Caenorhabditis inopinata, the closest known relative of C. elegans, using live-cell imaging and functional perturbation. We found that C. inopinata embryos exhibit altered pronuclear migration, reduced anaphase spindle oscillations, and slower centrosome diffusion during telophase compared with C. elegans. These differences suggest weaker cortical pulling forces. Functional analyses using RNA interference showed that GPR retains its essential role in force generation, whereas the contribution of the microtubule depolymerizing kinesin KLP-7 is reduced in C. inopinata. Our results point to evolutionary changes in microtubule-regulated spindle dynamics, and provide insight into how conserved cellular processes can diversify through subtle changes in their underlying mechanisms.
SN  - 1932-6203
ER  -