Specific regulation of CENP-E and kinetochores during meiosis I/meiosis II transition in pig oocytes

Lee, Jibak; Miyano, Takashi; Dai, Yanfeng; Wooding, Peter; Yen, Tim J.; Moor, R. M.

doi:10.1002/(sici)1098-2795(200005)56:1<51::aid-mrd7>3.0.co;2-n

Cited by 35 publications

(12 citation statements)

References 54 publications

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“…Thus, the monopolar attachment in budding yeast might be caused by the 'fusion' of point centromeres (a pair of sister kinetochores behaves as a single kinetochore), or inactivation of one of the two sister kinetochores in a pair (Monje-Casas et al 2007). In contrast to budding yeast, both sister kinetochores are captured by multiple microtubules in most other eukaryotes; electron-microscopic analyses reveal that sister kinetochores are arranged side-by-side, and both are attached to microtubules during meiosis I (Goldstein 1981;Moore and Orr-Weaver 1998;Lee et al 2000;Parra et al 2004).…”

Section: Mono-orientation Of Kinetochores During Meiosis Imentioning

confidence: 99%

Studies of meiosis disclose distinct roles of cohesion in the core centromere and pericentromeric regions

Sakuno

Watanabe

2009

Chromosome Res

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During meiosis, a single round of genome duplication is followed by two sequential rounds of chromosome segregation. Through this process, a diploid parent cell generates gametes with a haploid set of chromosomes. A characteristic of meiotic chromosome segregation is a stepwise loss of sister chromatid cohesion along chromosomal arms and at centromeres. Whereas arm cohesion plays an important role in ensuring homologue disjunction at meiosis I, persisting cohesion at pericentromeric regions throughout meiosis I is essential for the faithful equational segregation of sisters in the following meiosis II, similar to mitosis. A widely conserved pericentromeric protein called shugoshin, which associates with protein phosphatase 2A (PP2A), plays a critical role in this protection of cohesin. Another key aspect of meiosis I is the establishment of monopolar attachment of sister kinetochores to spindle microtubules. Cohesion or physical linkage at the core centromeres, where kinetochores assemble, may conjoin sister kinetochores, leading to monopolar attachment. A meiosis-specific kinetochore factor such as fission yeast Moa1 or budding yeast monopolin contributes to this regulation. We propose that cohesion at the core centromere and pericentromeric regions plays distinct roles, especially in defining the orientation of kinetochores.

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Section: Mono-orientation Of Kinetochores During Meiosis Imentioning

confidence: 99%

Studies of meiosis disclose distinct roles of cohesion in the core centromere and pericentromeric regions

Sakuno

Watanabe

2009

Chromosome Res

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“…In the oocytes maturing to the metaphase II (MII) stage, the shape and size of the meiotic spindle as well as chromosomal alignment were imaged by ␤-tubulin and nuclear DNA staining as previously described [36][37][38]. Oocytes were fixed in 4% paraformaldehyde in Dulbecco PBS (Invitrogen) containing 0.1% polyvinyl alcohol (PVA; Sigma) for 40 min at 37ЊC followed by treatment with 0.2% Triton X-100 (Sigma) in PBS-PVA for 40 min.…”

Section: Assessment Of Spindle Structure By Immunofluorescent Studymentioning

confidence: 99%

Effect of Treating Induced Mitochondrial Damage on Embryonic Development and Epigenesis

Takeuchi

Neri

Katagiri

et al. 2005

Biology of Reproduction

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Germinal vesicle transplantation (GVT) has been proposed as a possible treatment to correct age-related oocyte aneuploidy caused by dysfunctional ooplasm. How healthy ooplasm regulates normal meiosis and subsequent development has yet to be elucidated, but impaired mitochondrial metabolism may be attributable to incomplete segregation of the oocyte chromosomes. In the present study, after ooplasmic mitochondrial damage by photoirradiating chloromethyl-X-rosamine, examination of the oocyte nuclei's ability to survive after transfer into healthy ooplasts was performed. To assess their fertilizability and potential for development, GVT oocytes were fertilized by intracytoplasmic sperm injection (ICSI) and transferred to foster mice. Condition of the offspring at birth was assessed, and epigenetic analysis was performed. Photosensitization consistently inhibited oocyte maturation. However, after GVT of photosensitized nuclei into healthy ooplasts, 67.2% were reconstituted, and 76.2% of these matured normally, with an overall rate of 51.2%, much higher than that (6.0%) in the mitochondrially injured oocytes. After ICSI, 65.8% (52/79) of GVT oocytes were fertilized normally, and 21.1% (11/52) eventually reached the blastocyst stage. The transfer of 132 two-cell GVT embryos into the oviducts of pseudopregnant females resulted in 17 apparently healthy live offspring. For some key developmental genes, a high level of expression was identified in the GVT and ''rescue''-derived fetal adnexa. Thus, one can induce in oocyte mitochondria a photosensitization-based type of damage, which consistently inhibits GV breakdown, meiotic spindle formation, chromosomal segregation, and polar body extrusion. Germinal vesicle transplanted and rescued oocytes were able to undergo maturation, fertilization, and embryonic cleavage and, ultimately, to develop to term. This approach may provide a model with which to study the age-related ooplasmic dysfunction seen in human oocytes.

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“…The other type represents transient proteins, such as CENP-E, CENP-F, MAD1, MAD2, BUB1, and BUB3. These proteins can be detected in the specific cell cycle, mostly in M-phase by specific antibodies [10][11][12][13][14][15]. When CREST was used to label the CENPs in the kinetochores, it was found that these CENPs were present throughout the meiosis of oocytes from germinal vesicle (GV) to metaphase II (M-II) 741 MAD2 IN RAT OOCYTES DURING MEIOSIS stages in mammalian oocytes [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

“…These transient proteins include mitotic arrest deficient 1 (MAD1), MAD2, MAD3 (BUBR1), budding uninhibited by benzimidazole 1 (BUB1), BUB3, and motor proteins, such as CENP-E, and cytoplasmic dynein. It has been found that most of these proteins are also located in the kinetochores and the activities of these proteins (kinases) are related to the chromosome movement and anaphase onset during mitosis [7,[10][11][12][13][14][15][19][20][21][22]. MAD2 is one of the proteins widely studied in mitosis.…”

Section: Introductionmentioning

confidence: 99%

Intra-oocyte Localization of MAD2 and Its Relationship with Kinetochores, Microtubules, and Chromosomes in Rat Oocytes During Meiosis1

Zhang

et al. 2004

Biology of Reproduction

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The present study was designed to investigate subcellular localization of MAD2 in rat oocytes during meiotic maturation and its relationship with kinetochores, chromosomes, and microtubules. Oocytes at germinal vesicle (GV), prometaphase I (ProM-I), metaphase I (M-I), anaphase I (A-I), telophase I (T-I), and metaphase II (M-II) were fixed and immunostained for MAD2, kinetochores, microtubules and chromosomes. The stained oocytes were examined by confocal microscopy. Some oocytes from GV to M-II stages were treated by a microtubule disassembly drug, nocodazole, or treated by a microtubule stabilizer, Taxol, before examination. Anti-MAD2 antibody was also injected into the oocytes at GV stage and the injected oocytes were cultured for 6 h for examination of chromosome alignment and spindle formation. It was found that MAD2 was at the kinetochores in the oocytes at GV and ProM-I stages. Once the oocytes reached M-I stage in which an intact spindle was formed and all chromosomes were aligned at the equator of the spindle, MAD2 disappeared. However, when oocytes from GV to M-II stages were treated by nocodazole, spindles were destroyed and MAD2 was observed in all treated oocytes. When nocodazole-treated oocytes at M-I and M-II stages were washed and cultured for spindle recovery, it was found that, once the relationship between microtubules and chromosomes was established, MAD2 disappeared in the oocytes even though some chromosomes were not aligned at the equator of the spindle. On the other hand, when oocytes were treated with Taxol, MAD2 localization was not changed and was the same as that in the control. However, immunoblotting of MAD2 indicated that MAD2 was present in the oocytes at all stages; nocodazole and Taxol treatment did not influence the quantity of MAD2 in the cytoplasm. Significantly higher proportions of anti-MAD2 antibody-injected oocytes proceeded to premature A-I stage and more oocytes had misaligned chromosomes in the spindles. The present study indicates that MAD2 is a spindle checkpoint protein in rat oocytes during meiosis. When the spindle was destroyed by nocodazole, MAD2 was reactivated in the oocytes to overlook the attachment between chromosomes and microtubules. However, in this case, MAD2 could not check unaligned chromosomes in the recovered spindles, suggesting that a normal chromosome alignment is maintained only in the oocytes without any microtubule damages during maturation.

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Specific regulation of CENP-E and kinetochores during meiosis I/meiosis II transition in pig oocytes

Cited by 35 publications

References 54 publications

Studies of meiosis disclose distinct roles of cohesion in the core centromere and pericentromeric regions

Studies of meiosis disclose distinct roles of cohesion in the core centromere and pericentromeric regions

Effect of Treating Induced Mitochondrial Damage on Embryonic Development and Epigenesis

Intra-oocyte Localization of MAD2 and Its Relationship with Kinetochores, Microtubules, and Chromosomes in Rat Oocytes During Meiosis1

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