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Updated: Dec 24, 2025

Multi-Photon Laser Ablation of Cytoplasmic Microtubule Organizing Centers in Mouse Oocytes
Published on: November 11, 2022
PLK1 is required for chromosome compaction and microtubule organization in mouse oocytes
Tara M Little1, Philip W Jordan1
1Biochemistry and Molecular Biology Department, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205.
Abstract:
Errors during meiotic resumption in oocytes can result in chromosome missegregation and infertility. Several cell cycle kinases have been linked with roles in coordinating events during meiotic resumption, including polo-like kinases (PLKs). Mammals express four kinase-proficient PLKs (PLK1-4). Previous studies assessing the role of PLK1 have relied on RNA knockdown and kinase inhibition approaches, as Plk1 null mutations are embryonically lethal. To further assess the roles of PLK1 during meiotic resumption, we developed a Plk1 conditional knockout (cKO) mouse to specifically mutate Plk1 in oocytes. Despite normal oocyte numbers and follicle maturation, Plk1 cKO mice were infertile. From analysis of meiotic resumption, Plk1 cKO oocytes underwent nuclear envelope breakdown with the same timing as control oocytes. However, Plk1 cKO oocytes failed to form compact bivalent chromosomes, and localization of cohesin and condensin were defective. Furthermore, Plk1 cKO oocytes either failed to organize α-tubulin or developed an abnormally small bipolar spindle. These abnormalities were attributed to aberrant release of the microtubule organizing center (MTOC) linker protein, C-NAP1, and the failure to recruit MTOC components and liquid-like spindle domain (LISD) factors. Ultimately, these defects result in meiosis I arrest before homologous chromosome segregation.
Insights
Polo-like kinase 1 (PLK1) is crucial for oocyte meiotic resumption. Conditional knockout of PLK1 in mice causes infertility due to defective chromosome organization and spindle formation during meiosis.
Area of Science:
- Cell Biology
- Reproductive Biology
- Genetics
Background:
- Meiotic errors in oocytes lead to chromosome missegregation and infertility.
- Polo-like kinases (PLKs), including PLK1, are implicated in meiotic resumption coordination.
- Previous studies on PLK1 function were limited by embryonic lethality of null mutations.
Purpose of the Study:
- To investigate the specific role of PLK1 in oocyte meiotic resumption using a conditional knockout mouse model.
- To elucidate the molecular mechanisms underlying PLK1-dependent meiotic progression.
Main Methods:
- Development of a conditional knockout (cKO) mouse model for targeted mutation of Plk1 in oocytes.
- Analysis of oocyte maturation, chromosome organization, spindle formation, and protein localization during meiotic resumption.
- Assessment of fertility in Plk1 cKO mice.
Main Results:
- Plk1 cKO mice exhibited infertility despite normal oocyte numbers and follicle maturation.
- Plk1 cKO oocytes showed defects in bivalent chromosome formation and cohesin/condensin localization.
- Abnormalities in α-tubulin organization and bipolar spindle formation were observed in Plk1 cKO oocytes.
- Aberrant release of C-NAP1 and impaired recruitment of MTOC components and LISD factors were identified.
Conclusions:
- PLK1 is essential for proper chromosome organization and spindle assembly during oocyte meiotic resumption.
- PLK1 regulates C-NAP1 release and MTOC/LISD factor recruitment, crucial for meiotic progression.
- Disruption of PLK1 function leads to meiosis I arrest and infertility.
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