Ricochet transcription of pachytene piRNA promoters in mammals
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ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR168631.fastq.gz | Fastqsanger.gz | |||
| ERR168632.fastq.gz | Fastqsanger.gz | |||
| ERR168633.fastq.gz | Fastqsanger.gz | |||
| ERR168634.fastq.gz | Fastqsanger.gz |
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Project description:The origin and stability of germline noncoding RNAs remain largely uncharacterized in mammals. Here, we demonstrate that the vast majority of pachytene piRNAs originate from less than 100 bi- and unidirectionally transcribed loci in the mouse genome. These loci show features characteristic of transcribed protein-coding genes, including primary transcription by RNA polymerase II, H3K4 trimethylation marking the transcription initiation site, and H3K36 trimethylation present at elongation regions in a highly tissue-specific manner. We identified MYBL1, a spermatocyte-enriched transcription factor, as a potential driver of piRNA precursor transcripts. By similarly mapping piRNA clusters in testes of dog and opossum, we revealed that the regulatory architectures generating piRNAs appear to be highly conserved in mammals. Finally, we discovered that apparently neutral chromosomal rearrangements in evolution can act as an unexpected mechanism to generate novel piRNA clusters in diverse mammals. Thus, our results demonstrate how an integrated, multi-species approach can help define the genomic features and evolutionary mechanisms underlying mammalian germline noncoding RNAs.
2015-09-01 | E-MTAB-1265 | biostudies-arrayexpress
Project description:In the fetal mouse testis, PIWI Interacting RNAs (piRNAs) guide PIWI proteins to silence transposons, but after birth, most post-pubertal pachytene piRNAs map to genome uniquely and are thought to regulate genes required for male fertility. In human males, the developmental classes, precise genomic origins, and transcriptional regulation of post-natal piRNAs remain undefined. Here, we demarcate the genes and transcripts that produce post-natal piRNAs in human juvenile and adult testes. As in mouse, A‑MYB in humans drives transcription of both pachytene piRNA precursor transcripts and the mRNAs encoding piRNA biogenesis factors. Although human piRNA genes are syntenic to those in other placental mammals, their sequences are poorly conserved. In fact, pachytene piRNA loci are rapidly diverging even among modern humans. Our findings suggest that during mammalian evolution, pachytene piRNA genes are under fewer selective constraints. We speculate that pachytene piRNA diversity may provide a hitherto unrecognized driver of reproductive isolation.
2019-12-23 | GSE135791 | GEO
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals.
2013-03-26 | GSE44654 | GEO
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals.
2013-03-26 | GSE44588 | GEO
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals.
2013-03-27 | GSE45049 | GEO
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals. Transcriptome and ChIP sequencing in mouse and rooster testes
2013-03-26 | E-GEOD-44654 | biostudies-arrayexpress
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals. ChIP sequencing in mouse and rooster testes.
2013-03-26 | E-GEOD-44588 | biostudies-arrayexpress
Project description:Animal germ cells produce PIWI-interacting RNAs (piRNAs), small silencing RNAs that suppress transposons and enable gamete maturation. Mammalian transposon-silencing piRNAs accumulate early in spermatogenesis, whereas pachytene piRNAs are produced later during post-natal spermatogenesis and account for >95% of all piRNAs in the adult mouse testis. Mutants defective for pachytene piRNA pathway proteins fail to produce mature sperm, but neither the piRNA precursor transcripts nor the trigger for pachytene piRNA production is known. Here, we show that the transcription factor A-MYB initiates pachytene piRNA production. A-MYB drives transcription of both pachytene piRNA precursor RNAs and the mRNAs for core piRNA biogenesis factors, including MIWI, the protein through which pachytene piRNAs function. A-MYB regulation of piRNA pathway proteins and piRNA genes creates a coherent feed-forward loop that ensures the robust accumulation of pachytene piRNAs. This regulatory circuit, which can be detected in rooster testes, likely predates the divergence of birds and mammals. smallRNA-Seq in mouse and rooster testes
2013-03-27 | E-GEOD-45049 | biostudies-arrayexpress
Project description:Pachytene piRNAs control male fertility across metazoans, yet mechanisms through which they govern meiosis I in pachytene remain unclear. We demonstrate, in C. elegans, that homolog pairing, and crossover formation are compromised in the absence of piRNA function. We identify several protein coding genes as targets of piRNAs including Polo like kinase 3 (PLK-). Pachytene piRNAs spatially restrict and exclude PLK-3 expression from meiosis I. Expansion of PLK-3 expression into the pachytene region, upon loss of piRNAs, is reflected in meiotic defects, which are partially rescued by removal of ectopic PLK-3. Pachytene piRNAs regulate PLK-3 through both translational repression and post-transcriptional degradation establishing the spatiotemporal control of gene expression. Given the conserved role of pachytene piRNAs, we propose that these mechanisms may be applicable to mammals.
2023-10-14 | GSE245023 | GEO
Project description:In the male germ cells of eutherian animals, 26–30-nt-long PIWI-interacting RNAs (piRNAs) emerge when spermatocytes enter the pachytene phase of meiosis. These pachytene piRNAs derive from ~100 discrete autosomal loci resemble canonical protein-coding genes and long non-coding RNA-producing genes—they are transcribed by RNA polymerase II, bearing 5´ caps and 3´ poly(A) tails, and their transcripts often contain introns that are removed before nuclear export and processing into piRNAs. However, it is unclear which genic and epigenetic features distinguish pachytene piRNA genes from other types of genes and dictate their germline-specific expression. We report that an unusually long first exon (≥ 10 kb) or a long gene absent of introns altogether is highly correlated with both the germline-specific production of piRNA precursor transcripts from mouse pachytene piRNA loci. We also found that these precursor transcripts are enriched in the binding by THOC1 (also known as HPR1) and THOC2, subunits of the THO complex critical for transcription elongation and nuclear export of mRNAs. Our integrative analysis of transcriptome, piRNA, and epigenome datasets across multiple species reveals that a long first exon is an evolutionarily conserved feature of pachytene piRNA loci. We further found that a highly methylated promoter, often containing a low or intermediate level of CG dinucleotides, correlates with germline expression and somatic silencing of pachytene piRNA loci.
2020-10-24 | GSE147724 | GEO