Epigenetic modification during oocyte growth and maturation

2006 ◽  
pp. 124-125
Keyword(s):  
Epigenetic Modification ◽  
Oocyte Growth

scholarly journals Alterations in epigenetic modifications during oocyte growth in mice

Reproduction ◽  
2007 ◽  
Vol 133 (1) ◽  
pp. 85-94 ◽  
Author(s):  
Shun-ichiro Kageyama ◽  
Honglin Liu ◽  
Naoto Kaneko ◽  
Masatoshi Ooga ◽  
Masao Nagata ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Modifications ◽  
Epigenetic Modification ◽  
Germinal Vesicle ◽  
Epigenetic Modifications ◽  
Condensed Chromatin ◽  
Rt Pcr ◽  
Oocyte Growth ◽  
Lysine Residues ◽  
Signal Intensities

During oocyte growth, chromatin structure is altered globally and gene expression is silenced. To investigate the involvement of epigenetic modifications in the regulation of these phenomena, changes in global DNA methylation and in various histone modifications, i.e. acetylation of H3K9, H3K18, H4K5, and H4K12, and methylation of H3K4 and H3K9, were examined during the growth of mouse oocytes. Immunocytochemical analysis revealed that the signal intensities of all these modifications increased during growth and that fully grown, germinal vesicle (GV)-stage oocytes showed the most modifications. Since acetylation of most of the lysine residues on histones and methylation of H3K4 are associated with active gene expression, the increased levels of these modifications do not seem to be associated with gene silencing in GV-stage oocytes. Given that there are two types of GV-stage oocytes with different chromatin configurations and transcriptional activities, the epigenetic modification statuses of these two types were compared. The levels of all the epigenetic modifications examined were higher in the SN(surrounded nucleolus)-type oocytes, in which highly condensed chromatin is concentrated in the area around the nucleolus and gene expression is silenced than in the NSN(not surrounded nucleolus)-type oocytes, in which less-condensed chromatin does not surround the nucleolus and gene expression is active. In addition, the expression levels of various enzymes that catalyze histone modifications were shown by RT-PCR to increase with oocyte growth. Taken together, the results show that all of the epigenetic modifications increased in a concerted manner during oocyte growth, and suggest that these increases are not associated with gene expression.

scholarly journals Probiotic Administration Mitigates Bisphenol A Reproductive Toxicity in Zebrafish

2021 ◽  
Vol 22 (17) ◽  
pp. 9314
Author(s):  
Christian Giommi ◽  
Hamid R. Habibi ◽  
Michela Candelma ◽  
Oliana Carnevali ◽  
Francesca Maradonna
Keyword(s):  
Bisphenol A ◽  
Epigenetic Modification ◽  
Reproductive Toxicity ◽  
Final Concentration ◽  
Class Iii ◽  
Oocyte Growth ◽  
Endocrine Disrupting Compound ◽  
Probiotic Strains ◽  
Set Up ◽  
Key Aspects

Although the use of bisphenol A (BPA) has been banned in a number of countries, its presence in the environment still creates health issues both for humans and wildlife. So far, BPA toxicity has been largely investigated on different biological processes, from reproduction to development, immune system, and metabolism. In zebrafish, Danio rerio, previous studies revealed the ability of environmentally relevant concentrations of this contaminant to significantly impair fertility via epigenetic modification. In addition, several studies demonstrated the ability of different probiotic strains to improve organism health. This study provides information on the role of the probiotic mixture SLAb51 to counteract adverse BPA effects on reproduction. A 28-day trial was set up with different experimental groups: BPA, exposed to 10 µg/L BPA; P, receiving a dietary supplementation of SLAb51 at a final concentration of 109 CFU/g; BPA+P exposed to 10 µg/L BPA and receiving SLAb51 at a final concentration of 109 CFU/g and a C group. Since oocyte growth and maturation represent key aspects for fertility in females, studies were performed on isolated class III (vitellogenic) and IV (in maturation) follicles and liver, with emphasis on the modulation of the different vitellogenin isoforms. In males, key signals regulating spermatogenesis were investigated. Results demonstrated that in fish exposed to the combination of BPA and probiotic, most of the transcripts were closer to C or P levels, supporting the hypothesis of SLAb51 to antagonize BPA toxicity. This study represents the first evidence related to the use of SLAb51 to improve reproduction and open new fields of investigation regarding its use to reduce endocrine disrupting compound impacts on health.

scholarly journals Cyclophosphamide Exposure Causes Long-Term Detrimental Effect of Oocytes Developmental Competence Through Affecting the Epigenetic Modification and Maternal Factors’ Transcription During Oocyte Growth

2021 ◽  
Vol 9 ◽  
Author(s):  
Weijie Yang ◽  
Yerong Ma ◽  
Jiamin Jin ◽  
Peipei Ren ◽  
Hanjing Zhou ◽  
...  
Keyword(s):  
Dna Damage ◽  
Culture Media ◽  
Epigenetic Modification ◽  
Primordial Follicle ◽  
Oocyte Quality ◽  
Mature Oocyte ◽  
Developmental Competence ◽  
Oocyte Growth ◽  
Primordial Follicles

Cyclophosphamide (CTX) is widely used in various cancer therapies and in immunosuppression, and patients can still have babies after CTX chemotherapy. CTX directly causes primordial follicle loss with overactivation and DNA damage-induced apoptosis. Previous studies have shown that maternal exposure to CTX before conception increases the incidence of birth abnormalities and alters the methylation of genes in the oocytes of offspring. Mice were treated with a single dose of CTX (100 mg/kg) at post-natal day 21 and sacrificed 47 days later when primordial follicles surviving chemotherapy developed to the antral stage. Acute DNA damage and acceleration of the activation of primordial follicles after CTX treatment were repaired within several days, but the remaining follicle numbers remarkably decrease. Although partial surviving primordial follicle were developed to mature oocyte, oocyte quality hemostasis was impaired exhibiting aberrant meiosis progression, abnormal spindle and aneuploidy, mitochondrial dysfunction and increased endoplasmic reticulum stress. Thereafter, embryo development competency significantly decreased with fewer blastocyst formation after CTX exposure. CTX treatment resulted in alteration of DNA methylations and histone modifications in fully grown GV oocytes. Single-cell RNA-seq revealed CTX treatment suppressed multiple maternal genes’ transcription including many methyltransferases and maternal factor YAP1, which probably accounts for low quality of CTX-repaired oocyte. In vitro addition of lysophosphatidic acid (LPA) to embryo culture media to promote YAP1 nuclear localization improved CTX-repaired embryo developmental competence. This study provides evidence for the consistent toxic effect of CTX exposure during follicle development, and provide a new mechanism and new insights into future clinical interventions for fertility preservation.

Genetic modification for bimaternal embryo development

2009 ◽  
Vol 21 (1) ◽  
pp. 31 ◽  
Author(s):  
Tomohiro Kono
Keyword(s):  
Embryo Development ◽  
Genetic Modification ◽  
Direct Evidence ◽  
Epigenetic Modification ◽  
Growth Period ◽  
Epigenetic Modifications ◽  
Imprinted Genes ◽  
Mammalian Development ◽  
Oocyte Growth ◽  
Paternal Contribution

Full mammalian development typically requires genomes from both the oocyte and spermatozoon. Biparental reproduction is necessary because of parent-specific epigenetic modification of the genome during gametogenesis; that is, a maternal methylation imprint imposed during the oocyte growth period and a paternal methylation imprint imposed in pregonadal gonocytes. This leads to unequivalent expression of imprinted genes from the maternal and paternal alleles in embryos and individuals. It is possible to hypothesise that the maternal methylation imprint is necessary to prevent parthenogenesis, which extinguishes the opportunity for having descendents, whereas the paternal methylation imprint prevents parthenogenesis, ensuring that a paternal contribution is obligatory for any descendants. To date, there are several lines of direct evidence that the epigenetic modifications that occur during oocyte growth have a decisive effect on mammalian development. Using bimaternal embryos with two sets of maternal genomes, the present paper illustrates how parental methylation imprints are an obstacle to the progression of parthenogenesis.

Search for novel metabolites in fungal endophytes: study of Phomopsis sp. and Colletotrichum sp. co-cultivation and Botryosphaeria mamane epigenetic modification

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
A Triastuti ◽  
M Vansteelandt ◽  
F Barakat ◽  
P Jargeat ◽  
L Rieusset ◽  
...  
Keyword(s):  
Epigenetic Modification ◽  
Fungal Endophytes

Genome-wide reprogramming by DNA demethylation during mouse oocyte growth and early development

2014 ◽  
Author(s):  
Akihiko Sakashita ◽  
Yosuke Iseki ◽  
Mei Nakajima ◽  
Takuya Wakai ◽  
Hisato Kobayashi ◽  
...  
Keyword(s):  
Early Development ◽  
Dna Demethylation ◽  
Mouse Oocyte ◽  
Oocyte Growth ◽  
Genome Wide

Epigenetic Modification of Nociceptive Mediators: Implications for the Etiology of Neural Hypersensitivity (Part I)

2015 ◽  
Vol 12 (1) ◽  
pp. 384-390
Author(s):  
Mary Pathak ◽  
◽  
Liming Lei ◽  
Nan Wang ◽  
Maria Bolick ◽  
...  
Keyword(s):  
Epigenetic Modification

Examination of the dynamics of global DNA methylation pattern establishment during spermatogenesiss

2007 ◽  
Vol 30 (4) ◽  
pp. 90
Author(s):  
Kirsten Niles ◽  
Sophie La Salle ◽  
Christopher Oakes ◽  
Jacquetta Trasler
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Epigenetic Modification ◽  
Methylation Pattern ◽  
Chromosome 9 ◽  
Specific Gene ◽  
Global Methylation ◽  
Dna Methylation Pattern ◽  
Methylation Patterns

Background: DNA methylation is an epigenetic modification involved in gene expression, genome stability, and genomic imprinting. In the male, methylation patterns are initially erased in primordial germ cells (PGCs) as they enter the gonadal ridge; methylation patterns are then acquired on CpG dinucleotides during gametogenesis. Correct pattern establishment is essential for normal spermatogenesis. To date, the characterization and timing of methylation pattern acquisition in PGCs has been described using a limited number of specific gene loci. This study aimed to describe DNA methylation pattern establishment dynamics during male gametogenesis through global methylation profiling techniques in a mouse model. Methods: Using a chromosome based approach, primers were designed for 24 regions spanning chromosome 9; intergenic, non-repeat, non-CpG island sequences were chosen for study based on previous evidence that these types of sequences are targets for testis-specific methylation events. The percent methylation was determined in each region by quantitative analysis of DNA methylation using real-time PCR (qAMP). The germ cell-specific pattern was determined by comparing methylation between spermatozoa and liver. To examine methylation in developing germ cells, spermatogonia from 2 day- and 6 day-old Oct4-GFP (green fluorescent protein) mice were isolated using fluorescence activated cell sorting. Results: As compared to liver, four loci were hypomethylated and five loci were hypermethylated in spermatozoa, supporting previous results indicating a unique methylation pattern in male germ cells. Only one region was hypomethylated and no regions were hypermethylated in day 6 spermatogonia as compared to mature spermatozoa, signifying that the bulk of DNA methylation is established prior to type A spermatogonia. The methylation in day 2 spermatogonia, germ cells that are just commencing mitosis, revealed differences of 15-20% compared to day 6 spermatogonia at five regions indicating that the most crucial phase of DNA methylation acquisition occurs prenatally. Conclusion: Together, these studies provide further evidence that germ cell methylation patterns differ from those in somatic tissues and suggest that much of methylation at intergenic sites is acquired during prenatal germ cell development. (Supported by CIHR)

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