The Effect of Epigenetic Changes on the Extrusion of the First Polar Body in Pig Oocytes During In Vitro Maturation.
Cell Reprogram
; 21(3): 129-140, 2019 06.
Article
en En
| MEDLINE
| ID: mdl-31084435
The present study was designed to investigate the comprehensive function of maternal factors of primordial germ cell 7 (PGC7) and POU5F1-POU class 5 homeobox 1 (OCT4), as well as the epigenetic modification roles on the mitosis for the extrusion of first polar body (PB1) in pig maturated oocytes. First, the common distribution of histone modifications, including H3K4me2, H3K27me3, H3K9me2, and H4K12ac and DNA methylation, were detected at the high level in the nucleus. However, only one part of the chromosome was higher methylated or acetylated when the mitosis happened to extrude the PB1. When the mitosis was inhibited by the cytochalasin B (CB) treatment, the expression of PGC7, OCT4, DNA methyltransferase1 (DNMT1), DNA methyltransferase3b (DNMT3b), tet methylcytosine dioxygenase 1 (TET1), tet methylcytosine dioxygenase 2 (TET2), and tet methylcytosine dioxygenase 3 (TET3) could be inhibited (p < 0.01), and no concentrated expression of the PGC7 and OCT4 was observed on the chromosome, but the levels of H3K9me2 and H4K12ac were higher. In addition, when the trichostatin A was performed on the in vitro maturation, the extrusion of the PB1 was inhibited too. And the histone methylation (H3K9me2 and H3K27me3) could be detected all the time with relative higher level and no demethylation could be observed. However, the expression of PGC7 and OCT4 was lower in the chromosome. It might indicate that the maternal factor of PGC7 and histone modification that included H4K12ac and H3K9me2 could regulate the extrusion of the PB1 and play an important role in the maturation of pig oocytes.
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Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Metilación de ADN
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Sus scrofa
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Epigénesis Genética
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Factor 3 de Transcripción de Unión a Octámeros
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Cuerpos Polares
Límite:
Animals
Idioma:
En
Revista:
Cell Reprogram
Año:
2019
Tipo del documento:
Article