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Updated: Jun 8, 2026
Meiotic Spindle Assessment in Mouse Oocytes by siRNA-mediated Silencing
Published on: October 11, 2015
p38α MAPK is a MTOC-associated protein regulating spindle assembly, spindle length and accurate chromosome
Xiang-Hong Ou1, Sen Li, Bao-Zeng Xu
1Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract:
P38αMAPK (p38α) is usually activated in response to various stresses and plays a role in the inhibition of cell proliferation and tumor progression, but little is known about its roles in meiotic spindle assembly. In this study, we characterized the dynamic localization of p38α and explored its function in mouse oocyte meiotic maturation. P38α specifically colocalized with γ-tubulin and Plk1 at the center of MTOCs and spindle poles. Depletion of p38α by specific morpholino injection resulted in severely defective spindles and misaligned chromosomes probably via MK2 dephosphorylation. Notably, depletion of p38α led to significant spindle pole defects, spindle elongation, non-tethered kinetochore microtubules and increased microtubule tension. The disruption of spindle stability was coupled with decreased γ-tubulin and Plk1 at MTOCs. Overexpression of Eg5, a conserved motor protein, also caused spindle elongation and its morpholino injection almost completely rescued spindle elongation caused by p38α depletion. In addition, p38α-depletion decreased BubR1 and interfered with spindle assembly checkpoint (SAC), which resulted in aneuploid oocytes. Together, these data indicate that p38α is an important component of MTOCs, which regulates spindle assembly and spindle length, as well as stabilizes the spindle and spindle poles. Perturbed SAC and abnormal microtubule tension may be responsible for the misaligned chromosomes and high aneuploidy in p38α-depleted mouse oocytes.
Insights
P38αMAPK (p38α) is crucial for mouse oocyte meiotic maturation, regulating spindle assembly and stability. Its depletion causes defective spindles and aneuploidy by affecting microtubule organization and the spindle assembly checkpoint.
Area of Science:
- Cell Biology
- Molecular Biology
- Reproductive Biology
Background:
- P38αMAPK (p38α) is activated by stress and influences cell proliferation and tumor progression.
- Its specific role in meiotic spindle assembly remains largely uncharacterized.
Purpose of the Study:
- To investigate the dynamic localization and function of p38α during mouse oocyte meiotic maturation.
- To elucidate the mechanisms by which p38α regulates meiotic spindle formation and chromosome alignment.
Main Methods:
- Morpholino-mediated depletion of p38α in mouse oocytes.
- Immunofluorescence microscopy to visualize p38α, tubulin, and other key proteins.
- Analysis of spindle morphology, chromosome alignment, and spindle assembly checkpoint (SAC) function.
Main Results:
- P38α colocalizes with γ-tubulin and Plk1 at microtubule-organizing centers (MTOCs) and spindle poles.
- p38α depletion leads to defective spindles, chromosome misalignment, spindle elongation, and increased microtubule tension.
- Reduced p38α impairs SAC function and results in aneuploid oocytes, potentially via MK2 dephosphorylation and decreased BubR1 levels.
- Eg5 motor protein activity is implicated in the spindle elongation observed upon p38α depletion.
Conclusions:
- P38α is essential for regulating spindle assembly, spindle length, and spindle pole stability in mouse oocytes.
- Dysregulation of p38α impacts microtubule dynamics, SAC function, and chromosome segregation, leading to aneuploidy.
- P38α plays a critical role in ensuring accurate meiotic maturation and preventing aneuploidy.
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