Transcription of the Mouse Oocyte Genome

Moore, G. P. M.; Lintern‐Moore, Sue

doi:10.1095/biolreprod18.5.865

Cited by 65 publications

(30 citation statements)

References 26 publications

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“…Oocyte growth is accompanied by dramatic changes in gene expression, but starting at approximately midgrowth phase, transcription decreases such that full-grown oocytes are essentially transcriptionally inactive (3), and transcriptional quiescence appears critical for acquisition of developmental competence (4). Transcriptional quiescence is associated with chromatin condensation as well as changes in histone posttranslational modifications (PTMs) (5); histone PTMs such as phosphorylation, methylation, ubiquitination, and acetylation are intimately linked to transcriptional regulation and required for many biological processes (6,7), with histone acetylation typically associated with transcriptionally permissive chromatin (8).…”

mentioning

confidence: 99%

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Pan

Montgomery

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

122

130

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Dramatic changes in chromatin structure and histone modification occur during oocyte growth, as well as a global cessation of transcription. The role of histone modifications in these processes is poorly understood. We report the effect of conditionally deleting Hdac1 and Hdac2 on oocyte development. Deleting either gene has little or no effect on oocyte development, whereas deleting both genes results in follicle development arrest at the secondary follicle stage. This developmental arrest is accompanied by substantial perturbation of the transcriptome and a global reduction in transcription even though histone acetylation is markedly increased. There is no apparent change in histone repressive marks, but there is a pronounced decrease in histone H3K4 methylation, an activating mark. The decrease in H3K4 methylation is likely a result of increased expression of Kdm5b because RNAi-mediated targeting of Kdm5b in double-mutant oocytes results in an increase in H3K4 methylation. An increase in TRP53 acetylation also occurs in mutant oocytes and may contribute to the observed increased incidence of apoptosis. Taken together, these results suggest seminal roles of acetylation of histone and nonhistone proteins in oocyte development.O ogenesis is a protracted process that encompasses meiosis and oocyte growth, and results in the only cell that, following fertilization, can develop into an organism (1). In mice, at approximately day 13.5 of gestation, oogonia undergo a final round of DNA replication and enter the first meiotic prophase, at which point they are called oocytes. By the time of birth, oocytes are arrested in diplotene of the first meiotic prophase, are approximately 15 to 20 μm in diameter, and reside in primordial follicles in which the oocyte is surrounded by a single layer of flattened follicle cells. Oocyte growth is coordinated with follicle cell proliferation; the diameter of full-grown oocytes is approximately 80 μm. During the growth phase, oocytes acquire the ability to resume meiosis (i.e., acquisition of meiotic competence) and support development to term (i.e., acquisition of developmental competence). In vivo, release of gonadotropins triggers resumption of meiosis of full-grown oocytes present in preovulatory follicles with oocytes maturing to and arresting at metaphase II; fertilization triggers resumption and completion of meiosis (2).Oocyte growth is accompanied by dramatic changes in gene expression, but starting at approximately midgrowth phase, transcription decreases such that full-grown oocytes are essentially transcriptionally inactive (3), and transcriptional quiescence appears critical for acquisition of developmental competence (4). Transcriptional quiescence is associated with chromatin condensation as well as changes in histone posttranslational modifications (PTMs) (5); histone PTMs such as phosphorylation, methylation, ubiquitination, and acetylation are intimately linked to transcriptional regulation and required for many biological processes (6, 7), with histone acetylation ...

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mentioning

confidence: 99%

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Pan

Montgomery

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

122

130

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“…During folliculogenesis, oocyte growth is accompanied by a dramatic increase in gene transcription, a necessary step for the storage of proteins ensuring oocyte growth and dialogue with companion granulosa cells in addition to fertilization and embryo development. 3,4 Limited data are available concerning the transcriptional machinery and its regulation during oocyte growth. 5 Ovum mutant candidate gene 1 (Omcg1), also known as Ccdc16 and Zfp830, encodes a nuclear zinc finger protein involved in pre-mRNA processing including splicing 6 and transcription-coupled repair.…”

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confidence: 99%

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Vandormael-Pournin¹,

Guigon²,

Coudouel³

et al. 2014

Cell Death Differ

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Aberrant loss of oocytes following cancer treatments or genetic mutations leads to premature ovarian insufficiency (POI) associated with endocrine-related disorders in 1% of women. Therefore, understanding the mechanisms governing oocyte death is crucial for the preservation of female fertility. Here, we report the striking reproductive features of a novel mouse model of POI obtained through oocyte-specific inactivation (ocKO) of Omcg1/Zfp830 encoding a nuclear zinc finger protein involved in premRNA processing. Genetic ablation of OMCG1 in early growing oocytes leads to reduced transcription, accumulation of DNA double-strand breaks and subsequent c-Abl/TAp63-dependent oocyte death, thus uncovering the key role of OMCG1 for oocyte genomic integrity. All adult Omcg1 ocKO females displayed complete elimination of early growing oocytes and sterility. Unexpectedly, mutant females exhibited a normal onset of puberty and sexual receptivity. Detailed studies of Omcg1 ocKO ovaries revealed that the ovarian somatic compartment underwent a dramatic structural and functional remodeling. This allowed the cooperation between oocyte-depleted follicles and interstitial tissue to produce estradiol. Moreover, despite early folliculogenesis arrest, mutant mice exhibited sexual cyclicity as shown by cyclical changes in estrogen secretion, vaginal epithelium cytology and genital tract weight. Collectively, our findings demonstrate the key role of Omcg1 for oocyte survival and highlight the contribution of p63 pathway in damaged oocyte elimination in adulthood. Moreover, our findings challenge the prevailing view that sexual cyclicity is tightly dependent upon the pace of folliculogenesis and luteal differentiation.

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“…As more and more pro-hormones, hormones (and their mRNAs, Einspanier et al, 1986) are discovered in the ovary some may be candidates as recently mentioned for the SRIF (pig, Mori et al, 1985) and for the anti-mullerian hormone (AMH) (rat, Takahashi et al, 1986 Lintern-Moore, 1978 ;Kaplan et al, 1982 ;Bachvarova et al, 1985). After the growth period a low rate of RNA synthesis is maintained, even if nucleolus compaction indicates that rRNA transcription is impaired.…”

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confidence: 99%

Mammalian oocyte maturation

Thibault¹,

Szöllősi²,

Gérard³

1987

Reprod. Nutr. Dévelop.

207

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Transcription of the Mouse Oocyte Genome

Abstract: Transcriptionof the oocyte genome has been measured during follicle growth in the mouse.

Cited by 65 publications

References 26 publications

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Mammalian oocyte maturation

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