scholarly journals GM130, a cis-Golgi protein, regulates meiotic spindle assembly and asymmetric division in mouse oocyte

Cell Cycle ◽  
2011 ◽  
Vol 10 (11) ◽  
pp. 1861-1870 ◽  
Author(s):  
Chun-Hui Zhang ◽  
Zhen-Bo Wang ◽  
Song Quan ◽  
Xin Huang ◽  
Jing-Shan Tong ◽  
...  
Keyword(s):  
Spindle Assembly ◽  
Asymmetric Division ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Golgi Protein

Nek2 and its substrate, centrobin/Nip2, are required for proper meiotic spindle formation of the mouse oocytes

Zygote ◽  
2010 ◽  
Vol 19 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Seongkeun Sonn ◽  
Goo Taeg Oh ◽  
Kunsoo Rhee
Keyword(s):  
Spindle Assembly ◽  
Early Embryogenesis ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Biological Functions ◽  
Spindle Formation ◽  
Mouse Oocytes ◽  
Early Embryos ◽  
Pericentriolar Material ◽  
Meiotic Spindles

SummaryA typical centrosome consists of a pair of centrioles embedded in a proteinous matrix called pericentriolar material. However, the centrosomes in the mouse oocytes and early embryos lack centrioles, but consist of the γ-tubulin-enriched vesicle aggregates. We previously revealed that Nek2 and centrobin/Nip2, a centrosomal substrate of Nek2, is critical for the mouse early embryogenesis, especially at the step of spindle assembly during mitosis. In order to expand our understanding of the biological functions of Nek2, we examined expression and knockdown phenotypes of Nek2 and its substrates, centrobin and C-Nap1, in the mouse oocyte. Nek2, centrobin and C-Nap1 in the mouse oocytes were also centrosomal. Suppression of Nek2 and its substrates did not affect meiotic resumption of the oocytes. However, meiosis of the Nek2- and centrobin-suppressed oocytes was not completed, but arrested with defects in spindle assembly. No visible phenotype was observed in the C-Nap1-suppressed oocytes. These results indicate that Nek2 is critical for proper assembly of the meiotic spindles. Centrobin may be a possible substrate of Nek2 responsible for the meiotic spindle assembly in the mouse oocytes.

mInscuteable regulates meiotic spindle organization during mouse oocyte meiotic maturation

Zygote ◽  
2019 ◽  
Vol 28 (1) ◽  
pp. 45-50
Author(s):  
Zhuoni Xiao ◽  
Jiali Peng ◽  
Meiting Xie ◽  
Jing Yang ◽  
Wangming Xu
Keyword(s):  
Oocyte Maturation ◽  
Germinal Vesicle ◽  
Asymmetric Division ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Meiotic Maturation ◽  
Cellular Polarity ◽  
Germinal Vesicle Breakdown ◽  
Key Events ◽  
Oocyte Meiotic Maturation

SummaryEstablishment of cellular polarity is one of the key events during oocyte maturation. Inscuteable (Insc) has been identified as a key regulator of cell polarity during asymmetric division in Drosophila. However, the function of its evolutionarily conserved mammalian homologue, mInscuteable (mInsc), in mouse meiotic maturation is not clear. In this study, we investigated the roles of mInsc in mouse oocyte maturation. mInsc was detected at all stages of oocyte maturation. The protein level of mInsc was slightly higher at the germinal vesicle breakdown (GVBD) stage and remained constant during mouse oocyte maturation. The subcellular localization of mInsc overlapped with spindle microtubules. Disruption of microtubules and microfilaments caused changes in the localization of mInsc. Depletion or overexpression of mInsc significantly decreased the maturation rates of mouse oocytes. Depletion of mInsc significantly affected asymmetric division, spindle assembly, alignments of chromosomes and actin cap formation. Taken together, our results demonstrated that mInsc regulates meiotic spindle organization during mouse meiotic maturation.

RAB35 depletion affects spindle formation and actin-based spindle migration in mouse oocyte meiosis

2019 ◽  
Vol 25 (7) ◽  
pp. 359-372 ◽  
Author(s):  
Yu Zhang ◽  
Xiang Wan ◽  
Hong-Hui Wang ◽  
Meng-Hao Pan ◽  
Zhen-Nan Pan ◽  
...  
Keyword(s):  
Asymmetric Cell Division ◽  
Polar Body ◽  
Asymmetric Division ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Spindle Formation ◽  
Oocyte Meiosis ◽  
Spindle Stability ◽  
Polar Body Extrusion ◽  
Cytoskeleton Dynamics

Abstract Mammalian oocyte maturation involves a unique asymmetric cell division, in which meiotic spindle formation and actin filament-mediated spindle migration to the oocyte cortex are key processes. Here, we report that the vesicle trafficking regulator, RAB35 GTPase, is involved in regulating cytoskeleton dynamics in mouse oocytes. RAB35 GTPase mainly accumulated at the meiotic spindle periphery and cortex during oocyte meiosis. Depletion of RAB35 by morpholino microinjection led to aberrant polar body extrusion and asymmetric division defects in almost half the treated oocytes. We also found that RAB35 affected SIRT2 and αTAT for tubulin acetylation, which further modulated microtubule stability and meiotic spindle formation. Additionally, we found that RAB35 associated with RHOA in oocytes and modulated the ROCK–cofilin pathway for actin assembly, which further facilitated spindle migration for oocyte asymmetric division. Importantly, microinjection of Myc-Rab35 cRNA into RAB35-depleted oocytes could significantly rescue these defects. In summary, our results suggest that RAB35 GTPase has multiple roles in spindle stability and actin-mediated spindle migration in mouse oocyte meiosis.

Bora regulates meiotic spindle assembly and cell cycle during mouse oocyte meiosis

2013 ◽  
Vol 80 (6) ◽  
pp. 474-487 ◽  
Author(s):  
Rui Zhai ◽  
Yi-Feng Yuan ◽  
Yi Zhao ◽  
Xiao-Ming Liu ◽  
Yan-Hong Zhen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Oocyte Meiosis

Activated proline-rich tyrosine kinase 2 regulates meiotic spindle assembly in the mouse oocyte

2017 ◽  
Vol 119 (1) ◽  
pp. 736-747 ◽  
Author(s):  
Xiao-Qian Meng ◽  
Bing Cui ◽  
Dong Cheng ◽  
Hui Lyu ◽  
Li-Gang Jiang ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Meiotic Spindle ◽  
Tyrosine Kinase 2

scholarly journals OLA1 is responsible for normal spindle assembly and SAC activation in mouse oocytes

2019 ◽  
Author(s):  
Di Xie ◽  
Juan Zhang ◽  
JinLi Ding ◽  
Jing Yang ◽  
Yan Zhang
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Immunofluorescent Staining ◽  
Germinal Vesicle Breakdown ◽  
Oocyte Meiosis ◽  
Polar Body Extrusion ◽  
Spread Analysis

Background. OLA1 is a member of the GTPase protein family, unlike other members, it can bind and hydrolyze ATP more efficiently than GTP. OLA1 participates in cell proliferation, oxidative response and tumorigenesis. However, whether OLA1 is also required for oocyte meiosis is still unknown. Methods. In this study, the localization, expression, and functions of OLA1 in the mouse oocyte meiosis were examined. Immunofluorescent and confocal microscopy were used to explore the location pattern of OLA1 in the mouse oocyte. Moreover, nocodazole treatment was used to confirm the spindle-like location of OLA1 during mouse meiosis. Western blot was used to explore the expression pattern of OLA1 in the mouse oocyte. Microinjection of siRNA was used to explore the OLA1 functions in the mouse oocyte meiosis. In addition, chromosome spreading was used to investigate the spindle assembly checkpoint (SAC) activity. Results. Immunofluorescent staining showed that OLA1 evenly distributed in the cytoplasm at germinal vesicle (GV) stage. After meiosis resumption (GVBD), OLA1 co-localized with spindles, which was further identified by nocodazole treatment experiments. Knockdown of OLA1 impaired the germinal vesicle breakdown progression and finally resulted in a lower polar body extrusion rate. Immunofluorescence analysis indicated that knockdown of OLA1 led to abnormal spindle assembly, which was evidenced by multipolar spindles in OLA1-RNAi-oocytes. After 6 h post-GVBD in culture, an increased proportion of oocyte which has precociously entered into anaphase/telephase I (A/TI) was observed in OLA1-knockdown oocytes, suggesting that loss of OLA1 resulted in the premature segregation of homologous chromosomes. In addition, the chromosome spread analysis suggested that OLA1 knockdown induced premature anaphase onset was due to the precocious inactivation of SAC. Taken together, we concluded that OLA1 plays important role in GVBD, spindle assembly and SAC activation maintenance in oocyte meiosis.

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