H2A.Z regulates transcription, oocyte maturation and female fertility in mouse [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1099292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28638021_1.fastq.gz | Fastqsanger.gz | |||
| SRR28638021_2.fastq.gz | Fastqsanger.gz | |||
| SRR28638024_1.fastq.gz | Fastqsanger.gz | |||
| SRR28638024_2.fastq.gz | Fastqsanger.gz | |||
| SRR28638025_1.fastq.gz | Fastqsanger.gz |
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Project description:H2A.Z regulates transcription, oocyte maturation and female fertility in mouse [RNA-seq]
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Project description:Histone variants differ from canonical histones in their ability to be incorporated into chromatin independently of S-phase. H2A.Z is an evolutionarily conserved histone variant that plays critical roles in transcription regulation. However, its roles during mammalian oogenesis, a unique developmental stage marked by dynamic transcription activity without DNA replication, remain elusive. In this study, we demonstrated that oocyte-specific depletion of H2A.Z results in profound epigenetic and transcriptional alterations, impeding oocyte meiosis II resumption in mice, causing female infertility. Mechanistically, H2A.Z in mouse oocytes is enriched at active promoters and enhancers. Interestingly, H2A.Z is depleted from CG-rich silenced promoters in fully-grown oocytes (FGOs), unlike that in growing oocytes, early embryos and mESCs. In FGOs, the presence of H2A.Z correlates with H3K27ac, except in regions with DNA methylation and H3K36me3. Depletion of H2A.Z leads to partial loss of H3K27ac at both promoters and enhancers, correlated with impaired gene expression. Consistent with a role in gene activation, H2A.Z in FGOs is widely acetylated at the promoters and enhancers. Together, our findings uncover an essential role of H2A.Z in oocyte maturation and activation of cis-regulatory elements.
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Project description:Histone variants differ from canonical histones in their ability to be incorporated into chromatin independently of S-phase. H2A.Z is an evolutionarily conserved histone variant that plays critical roles in transcription regulation. However, its roles during mammalian oogenesis, a unique developmental stage marked by dynamic transcription activity without DNA replication, remain elusive. In this study, we demonstrated that oocyte-specific depletion of H2A.Z results in profound epigenetic and transcriptional alterations, impeding oocyte meiosis II resumption in mice, causing female infertility. Mechanistically, H2A.Z in mouse oocytes is enriched at active promoters and enhancers. Interestingly, H2A.Z is depleted from CG-rich silenced promoters in fully-grown oocytes (FGOs), unlike that in growing oocytes, early embryos and mESCs. In FGOs, the presence of H2A.Z correlates with H3K27ac, except in regions with DNA methylation and H3K36me3. Depletion of H2A.Z leads to partial loss of H3K27ac at both promoters and enhancers, correlated with impaired gene expression. Consistent with a role in gene activation, H2A.Z in FGOs is widely acetylated at the promoters and enhancers. Together, our findings uncover an essential role of H2A.Z in oocyte maturation and activation of cis-regulatory elements.
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Project description:DIS3L2 clears terminal-uridylated RNA to ensure oocyte maturation and female fertility
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Project description:During mammalian oocyte development, transcriptome undergoes accumulation in the oocyte growth phase and elimination in the oocyte maturation phase. At the transition point between growth and maturation, which is the germinal vesicle intact oocyte (GV), terminal uridylation labels RNA for degradation. In our study, we show that a small cohort of RNA are polyadenylated after tail uridylation (defined as uridylated-poly(A) RNA). Upon genetic depletion of DIS3L2 (Dis3l2cKO) in mouse oocytes, uridylated-poly(A) RNA is extensively stabilized and dominates the oocyte transcriptome, which results in increased transcriptome in Dis3l2cKO oocytes. Consequently, Dis3l2cKO female mice are infertile and almost all oocytes are arrested at the GV stage. Uridylated-poly(A) RNA generally has shorter poly(A) tails and lower translation activity. The uridylated-poly(A) RNA in Dis3l2cKO oocytes not only generates from the insufficient RNA degradation, but also comes from the tail dynamics of RNA. Our study demonstrates more possibilities of RNA fates after being terminally uridylated, and highlights the role of DIS3L2 in safeguarding the transcriptome by degrading uridylated-poly(A) RNA.
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