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Updated: Jun 8, 2026

Using Mouse Oocytes to Assess Human Gene Function During Meiosis I
Published on: April 10, 2018
ERK3 is required for metaphase-anaphase transition in mouse oocyte meiosis
Sen Li1, Xiang-Hong Ou, Zhen-Bo Wang
1State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Abstract:
ERK3 (extracellular signal-regulated kinase 3) is an atypical member of the mitogen-activated protein (MAP) kinase family of serine/threonine kinases. Little is known about its function in mitosis, and even less about its roles in mammalian oocyte meiosis. In the present study, we examined the localization, expression and functions of ERK3 during mouse oocyte meiotic maturation. Immunofluorescent analysis showed that ERK3 localized to the spindles from the pre-MI stage to the MII stage. ERK3 co-localized with α-tubulin on the spindle fibers and asters in oocytes after taxol treatment. Deletion of ERK3 by microinjection of ERK3 morpholino (ERK3 MO) resulted in oocyte arrest at the MI stage with severely impaired spindles and misaligned chromosomes. Most importantly, the spindle assembly checkpoint protein BubR1 could be detected on kinetochores even in oocytes cultured for 10 h. Low temperature treatment experiments indicated that ERK3 deletion disrupted kinetochore-microtubule (K-MT) attachments. Chromosome spreading experiments showed that knock-down of ERK3 prevented the segregation of homologous chromosomes. Our data suggest that ERK3 is crucial for spindle stability and required for the metaphase-anaphase transition in mouse oocyte maturation.
Insights
Extracellular signal-regulated kinase 3 (ERK3) is essential for mouse oocyte meiosis. Its deletion impairs spindle stability and chromosome alignment, preventing successful cell division.
Area of Science:
- Cell Biology
- Molecular Biology
- Developmental Biology
Background:
- Extracellular signal-regulated kinase 3 (ERK3) is an atypical mitogen-activated protein (MAP) kinase.
- Its function in mammalian oocyte meiosis remains largely uncharacterized.
Purpose of the Study:
- To investigate the localization, expression, and function of ERK3 during mouse oocyte meiotic maturation.
Main Methods:
- Immunofluorescent analysis to determine ERK3 localization.
- Microinjection of ERK3 morpholino (MO) to assess functional roles.
- Taxol treatment and low-temperature experiments to evaluate spindle and kinetochore-microtubule (K-MT) attachments.
- Chromosome spreading assays to examine chromosome segregation.
Main Results:
- ERK3 localizes to spindle fibers and asters throughout mouse oocyte meiotic maturation.
- ERK3 deletion leads to MI stage arrest, spindle defects, chromosome misalignment, and disrupted K-MT attachments.
- ERK3 deficiency prevents homologous chromosome segregation and delays spindle assembly checkpoint protein (BubR1) kinetochore localization.
Conclusions:
- ERK3 is critical for maintaining spindle stability during mouse oocyte meiosis.
- ERK3 is required for the metaphase-anaphase transition, ensuring proper chromosome segregation.
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