Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1029730 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26426600_1.fastq.gz | Fastqsanger.gz | |||
| SRR26426600_2.fastq.gz | Fastqsanger.gz | |||
| SRR26426601_1.fastq.gz | Fastqsanger.gz | |||
| SRR26426601_2.fastq.gz | Fastqsanger.gz | |||
| SRR26426602_1.fastq.gz | Fastqsanger.gz |
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Project description:Accurate meiotic progression is important for gamete formation and the generation of genetic diversity. However, little is known about the identity of chromatin regulators that underlie mammalian meiosis in vivo. Here, we identify the multifaceted functions of the chromatin remodeler ZNHIT1 in governing meiosis. The expression of *Znhit1* gradually increases during the meiotic prophase, and *Znhit1* knockout in spermatocytes results in arrested pachytene development, impaired DNA double-strand break repair, and defective homologous recombination. Single-cell RNA sequencing and transcriptome analysis reveal that *Znhit1* loss dysregulates meiotic transcriptional programs at the pachytene stage. Chromatin immunoprecipitation data show that ZNHIT1 is needed for the incorporation of the histone variant H2A.Z into pachytene chromatin. Moreover, we found that H2A.Z cooperates with the transcription factor A-MYB to co-bind DNA elements and control gene activity. Our findings provide insights into the regulatory mechanisms governing meiotic progression and highlight ZNHIT1 as a critical regulator of meiotic progression.
2026-05-31 | GSE333549 | GEO
Project description:Accurate meiotic progression is important for gamete formation and the generation of genetic diversity. However, little is known about the identity of chromatin regulators that underlie mammalian meiosis in vivo. Here, we identify the multifaceted functions of the chromatin remodeler ZNHIT1 in governing meiosis. The expression of *Znhit1* gradually increases during the meiotic prophase, and *Znhit1* knockout in spermatocytes results in arrested pachytene development, impaired DNA double-strand break repair, and defective homologous recombination. Single-cell RNA sequencing and transcriptome analysis reveal that *Znhit1* loss dysregulates meiotic transcriptional programs at the pachytene stage. Chromatin immunoprecipitation data show that ZNHIT1 is needed for the incorporation of the histone variant H2A.Z into pachytene chromatin. Moreover, we found that H2A.Z cooperates with the transcription factor A-MYB to co-bind DNA elements and control gene activity. Our findings provide insights into the regulatory mechanisms governing meiotic progression and highlight ZNHIT1 as a critical regulator of meiotic progression.
2026-05-31 | GSE333548 | GEO
Project description:Accurate meiotic progression is important for gamete formation and the generation of genetic diversity. However, little is known about the identity of chromatin regulators that underlie mammalian meiosis in vivo. Here, we identify the multifaceted functions of the chromatin remodeler ZNHIT1 in governing meiosis. The expression of *Znhit1* gradually increases during the meiotic prophase, and *Znhit1* knockout in spermatocytes results in arrested pachytene development, impaired DNA double-strand break repair, and defective homologous recombination. Single-cell RNA sequencing and transcriptome analysis reveal that *Znhit1* loss dysregulates meiotic transcriptional programs at the pachytene stage. Chromatin immunoprecipitation data show that ZNHIT1 is needed for the incorporation of the histone variant H2A.Z into pachytene chromatin. Moreover, we found that H2A.Z cooperates with the transcription factor A-MYB to co-bind DNA elements and control gene activity. Our findings provide insights into the regulatory mechanisms governing meiotic progression and highlight ZNHIT1 as a critical regulator of meiotic progression.
2026-06-08 | GSE334745 | GEO
Project description:Accurate meiotic progression is important for gamete formation and the generation of genetic diversity. However, little is known about the identity of chromatin regulators that underlie mammalian meiosis in vivo. Here, we identify the multifaceted functions of the chromatin remodeler ZNHIT1 in governing meiosis. The expression of *Znhit1* gradually increases during the meiotic prophase, and *Znhit1* knockout in spermatocytes results in arrested pachytene development, impaired DNA double-strand break repair, and defective homologous recombination. Single-cell RNA sequencing and transcriptome analysis reveal that *Znhit1* loss dysregulates meiotic transcriptional programs at the pachytene stage. Chromatin immunoprecipitation data show that ZNHIT1 is needed for the incorporation of the histone variant H2A.Z into pachytene chromatin. Moreover, we found that H2A.Z cooperates with the transcription factor A-MYB to co-bind DNA elements and control gene activity. Our findings provide insights into the regulatory mechanisms governing meiotic progression and highlight ZNHIT1 as a critical regulator of meiotic progression.
2026-06-08 | GSE334744 | GEO
Project description:Accurate meiotic progression is important for gamete formation and the generation of genetic diversity. However, little is known about the identity of chromatin regulators that underlie mammalian meiosis in vivo. Here, we identify the multifaceted functions of the chromatin remodeler ZNHIT1 in governing meiosis. The expression of *Znhit1* gradually increases during the meiotic prophase, and *Znhit1* knockout in spermatocytes results in arrested pachytene development, impaired DNA double-strand break repair, and defective homologous recombination. Single-cell RNA sequencing and transcriptome analysis reveal that *Znhit1* loss dysregulates meiotic transcriptional programs at the pachytene stage. Chromatin immunoprecipitation data show that ZNHIT1 is needed for the incorporation of the histone variant H2A.Z into pachytene chromatin. Moreover, we found that H2A.Z cooperates with the transcription factor A-MYB to co-bind DNA elements and control gene activity. Our findings provide insights into the regulatory mechanisms governing meiotic progression and highlight ZNHIT1 as a critical regulator of meiotic progression.
2026-05-31 | GSE333547 | GEO
Project description:Regulation of the transcriptome to promote meiosis is important for sperm development and fertility. However, how chromatin remodeling directs the transcriptome during meiosis in male germ cells is largely unknown. Here, we demonstrate that the ISWI family ATP-dependent chromatin remodeling factor SMARCA5 (SNF2H) plays a critical role in regulating meiotic prophase progression during spermatogenesis. Males with germ cell-specific depletion of SMARCA5 are infertile and unable to form sperm. Loss of Smarca5 results in failure of meiotic progression with abnormal spermatocytes beginning at the pachytene stage and an aberrant global increase in chromatin accessibility, especially at genes important for meiotic prophase.
2024-12-05 | GSE279216 | GEO
Project description:Post-transcriptional regulation of gene expression by RNA-binding proteins helps facilitate fast, clean transitions from one cell state to the next during germ cell differentiation. Previously we showed that the RNA helicase YTHDC2 is required for germ cells to properly switch from mitosis to meiosis (Bailey et al., 2017). While YTHDC2 protein is first expressed as male germ cells enter meiosis, when it is needed to shut down the mitotic program, YTHDC2 expression continues to increase and reaches its highest levels later in meiotic prophase, in pachytene spermatocytes. Here we show that YTHDC2 has an additional essential role regulating meiotic progression in late spermatocytes during mouse germ cell differentiation. Inducing conditional knockout of Ythdc2 during the first wave of spermatogenesis, after the germ cells have already initiated meiotic prophase, allowed Ythdc2-deficient germ cells to successfully reach the pachytene stage and properly express many meiotic markers. However, instead of continuing through meiotic prophase and initiating the meiotic divisions, late pachytene spermatocytes failed to transition to the diplotene stage and quickly died. Loss of function of Ythdc2 in spermatocytes resulted in changes in transcript levels for a number of genes by RNA-sequencing compared to control spermatocytes. Our findings suggest that YTHDC2 facilitates proper progression of germ cells through multiple steps of meiosis, potentially via several mechanisms of post-transcriptional RNA regulation.
2023-03-02 | GSE222283 | GEO
Project description:Mammalian sexual reproduction critically relies on the generation of haploid gametes through a specialized cell division process known as meiosis. Here, we demonstrate that N-6 Adenine-Specific DNA methyltransferase 1 (N6AMT1) plays a crucial role in the progression of meiosis during spermatogenesis, as follows. Gene expression profiling revealed that N6AMT1 was expressed in germ cells throughout the entire process of spermatogenesis, with a peak in expression levels in spermatocytes at the prophase I stage of meiosis. Germ cell-specific deletion of N6amt1 in mice resulted in male subfertility as well as a significant reduction in sperm count. Notably, N6amt1-null spermatocytes exhibited meiotic arrest at prophase I and extensive apoptosis. Chromosome spreading assays revealed that N6amt1 loss impaired meiotic sex chromosome inactivation (MSCI) and delayed DNA double-strand break (DSB) repair, both crucial for proper meiotic progression. Correspondingly, transcriptomic analysis identified a substantial upregulation of genes mapping to sex chromosomes in N6amt1-null mutants, consistent with failures in MSCI. Moreover, N6AMT1 deficiency significantly augmented the expression of genes involved in the p53 pathway. Incorporating single-cell analysis, we found that the differentially expressed genes following the knockout of N6amt1 were primarily high-variability genes in pachytene stage spermatocytes, indicating that the absence of N6AMT1 leads to gene expression disorders during the pachytene stage. Taken together, our findings demonstrate that N6AMT1 is crucial to male fertility in mice, through molecular mechanisms for meiotic progression during spermatogenesis, including MSCI and DSB repair.
2025-05-30 | GSE283904 | GEO