SNPC-1.3 is a sex-specific transcription factor drives male piRNA expression in C. elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA640605 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12054100.fastq.gz | Fastqsanger.gz | |||
| SRR12054101.fastq.gz | Fastqsanger.gz | |||
| SRR12054102.fastq.gz | Fastqsanger.gz | |||
| SRR12054103.fastq.gz | Fastqsanger.gz | |||
| SRR12054104.fastq.gz | Fastqsanger.gz |
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Project description:Piwi-interacting RNAs (piRNAs) play essential roles in silencing repetitive elements to promote fertility in metazoans. Nearly one-third of the ~15,000 piRNA loci in the C. elegans hermaphrodite are enriched during spermatogenesis, whereas >2,000 piRNAs are enriched during oogenesis. However, the mechanism underlying this sex-specific regulation is unknown. Here we identify SNPC-1.3, a variant of a conserved subunit of the snRNA activating protein complex, as a male-specific piRNA transcription factor. Binding of SNPC-1.3 at male piRNA loci drives spermatogenic piRNA transcription and requires the core piRNA transcription factor SNPC-4. Loss of snpc-1.3 leads to depletion of spermatogenic piRNAs and defects in male-dependent fertility. Furthermore, TRA-1, a master regulator of sex determination, binds to the snpc-1.3 promoter and represses its expression during oogenesis. Loss of TRA-1 targeting causes ectopic expression of snpc-1.3 and male piRNAs during oogenesis. Thus, sexual dimorphic regulation of snpc-1.3 coordinates male and female piRNA expression during germline development.
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Project description:Piwi-interacting RNAs (piRNAs) play essential roles in silencing repetitive elements to promote fertility in metazoans. Studies in worms, flies, and mammals reveal that piRNAs are expressed in a sex-specific manner. However, the mechanisms underlying this sex-specific regulation are unknown. Here we identify SNPC-1.3, a male germline-enriched variant of a conserved subunit of the small nuclear RNA-activating protein complex, as a male-specific piRNA transcription factor in Caenorhabditis elegans. SNPC-1.3 colocalizes with the core piRNA transcription factor, SNPC-4, in nuclear foci of the male germline. Binding of SNPC-1.3 at male piRNA loci drives spermatogenic piRNA transcription and requires SNPC-4. Loss of snpc-1.3 leads to depletion of male piRNAs and defects in male-dependent fertility. Furthermore, TRA-1, a master regulator of sex determination, binds to the snpc-1.3 promoter and represses its expression during oogenesis. Loss of TRA-1 targeting causes ectopic expression of snpc-1.3 and male piRNAs during oogenesis. Thus, sexually dimorphic regulation of snpc-1.3 expression coordinates male and female piRNA expression during germline development.
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Project description:Transposable elements are genomic parasites that expand within and spread between genomes. Piwi proteins control transposon activity, notably in the germline. These proteins recognize their targets through small RNA co-factors named piRNAs, making piRNA biogenesis a key specificity-determining step in this important genome immunity system. While the processing of piRNA precursors is an essential step in this process, many molecular details of this process remain unknown. We identify a novel endoribonuclease, PUCH, that initiates piRNA processing in the nematode Caenorhabditis elegans. Genetic and biochemical studies show that PUCH, a trimer of Schlafen-like-domain (SLFNL) proteins, executes 5ï‚¢-end piRNA precursor cleavage. PUCH-mediated processing strictly requires an m7G-Cap and a Uracil at position three. We also demonstrate how PUCH interacts with PETISCO, a complex that binds piRNA precursors, and that this interaction enhances piRNA production in vivo. The identification of PUCH completes the C. elegans piRNA biogenesis repertoire and uncovers a novel type of RNA endonuclease formed by three SLFL proteins. Mammalian Slfn genes have been associated with immunity responses, exposing a novel molecular link between immune responses in mammals and deeply conserved RNA-based mechanisms that control transposable elements.
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Project description:Remarkably, tens of thousands of piwi-interacting RNAs (piRNAs) arise from a minimal number of discrete clustered regions in many organisms. However, it remains unclear if organization into these domains contributes to the highly coordinated, germline-specific expression of these small RNAs. Here, we show that SNPC-4, the DNA-binding subunit of the small nuclear RNA activating protein complex (SNAPc), binds piRNA clusters in a germline-specific manner and is required for global piRNA expression in C. elegans. Within piRNA domains, SNPC-4 not only binds at discrete sites through its established sequence motif, but also exhibits widely distributed binding across the region. Intriguingly, discrete peaks are not found at every piRNA, but instead occur frequently at Pol III-occupied tRNA genes, which have been previously implicated in chromatin organization. Given its unique binding pattern, we suggest that SNPC-4 promotes robust piRNA expression by establishing a permissive chromatin environment at clusters specifically in the germ line.
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Project description:PIWI-interacting RNAs (piRNAs) promote fertility in many animals. Yet, whether this is due to their conserved role in repressing repetitive elements (REs) or other functions remains unclear. Here, we show that the progressive loss of fertility in Caenorhabditis elegans lacking piRNAs is not caused by derepression of REs or other piRNA targets, but rather mediated by the epigenetic silencing of all the replicative histone genes. In the absence of piRNAs, downstream components of the piRNA pathway relocalize from germ granules and piRNA targets to histone mRNAs to synthesize antisense small RNAs (sRNAs) and induce transgenerational silencing. Removal of the downstream components of the piRNA pathway is sufficient to restore histone mRNA expression and fertility in piRNA mutants, and the inheritance of histone sRNAs in wild-type worms adversely affects their fertility for multiple generations. We conclude that the transgenerational silencing of histone genes contributes to the progressive loss of fertility in piRNA mutants and that coupling piRNAs and histone silencing may serve to maintain piRNAs production across evolution.
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