Planarians recruit piRNAs for mRNA turnover in adult stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA503908 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8162670.fastq.gz | Fastqsanger.gz | |||
| SRR8162680_1.fastq.gz | Fastqsanger.gz | |||
| SRR8162680_2.fastq.gz | Fastqsanger.gz | |||
| SRR8162690_1.fastq.gz | Fastqsanger.gz | |||
| SRR8162690_2.fastq.gz | Fastqsanger.gz |
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Project description:PIWI proteins utilize small RNAs called piRNAs to silence transposable elements, thereby protecting germline integrity. In planarian flatworms, PIWI proteins are essential for regeneration, which requires adult stem cells termed neoblasts. Here, we characterize planarian piRNAs and examine the roles of PIWI proteins in neoblast biology. We find that the planarian PIWI proteins SMEDWI-2 and SMEDWI-3 cooperate to degrade active transposons via the ping-pong cycle. Unexpectedly, we discover that SMEDWI-3 plays an additional role in planarian mRNA surveillance. While SMEDWI-3 degrades numerous neoblast mRNAs in a homotypic ping-pong cycle, it is also guided to another subset of neoblast mRNAs by antisense piRNAs and binds these without degrading them. Mechanistically, the distinct activities of SMEDWI-3 are primarily dictated by the degree of complementarity between target mRNAs and antisense piRNAs. Planarian PIWI proteins thus act as both nucleases and RNA-binding proteins, enabling planarians to repurpose piRNAs for critical roles in neoblast mRNA turnover.
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Project description:PIWI proteins utilize small RNAs called piRNAs to silence transposable elements, thereby protecting germline integrity. In planarian flatworms, PIWI proteins are essential for regeneration, which requires adult stem cells termed neoblasts. Here, we characterize planarian piRNAs and examine the roles of PIWI proteins in neoblast biology. We find that the planarian PIWI proteins SMEDWI-2 and SMEDWI-3 cooperate to degrade active transposons via the ping-pong cycle. Unexpectedly, we discover that SMEDWI-3 plays an additional role in planarian mRNA surveillance. While SMEDWI-3 degrades numerous neoblast mRNAs in a homotypic ping-pong cycle, it is also guided to another subset of neoblast mRNAs by antisense piRNAs and binds these without degrading them. Mechanistically, the distinct activities of SMEDWI-3 are primarily dictated by the degree of complementarity between target mRNAs and antisense piRNAs. Thus, PIWI proteins enable planarians to repurpose piRNAs for potentially critical roles in neoblast mRNA turnover.
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Project description:Small RNAs were deep sequenced from the liver and spleen of adult mice in an effort to identify somatic piRNAs. Following sequencing of all small RNAs, known non-coding RNAs were computationally removed from the dataset. The remaining RNAs were then mapped to the genome and analyzed for sequence characteristics (5' base, length) typical of known piRNAs. To determine if any of the identified small RNAs were MIWI2 dependent, we deep sequenced small RNAs from liver and spleen of MIWI2 KO mice and analyzed them as above.
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Project description:The goal of the study was to identify genes expressed in the proliferative cell population (neoblasts) of adult planarians. Proliferating cells are rapidly and specifically eliminated following lethal irradiation. Genes expressed by neoblasts, therefore, were expected to show decreased level of expression following 6,000 rads, relative to control animals. Total RNA was collected from control (unirradiated) animals and from animals 6, 12, 24, and 48 hours following 6,000 rads irradiation. Between three and five replicates were used for each sample
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Project description:Through integrated H2BGFP ChIP-seq data over multiple conditions and time points, as well as other related ChIP-seq and RNA-seq data in adult mouse heart. We observed genomewide and locus-specific H2B turnover in non-proliferating adult cardiomyocytes (Cms), and a majority of genomic regions with rapid turnover rates distributes on cis-regulatory elements, as well as these regions are associated with heart function, regulatory factors binding and their activities. Moreover, H2B turnover rate is always positively correlated with gene transcription level on enhancers, promoters and exons. The rapid turnover rates at cis-regulatory elements can be partially explained by the binding and co-binding of RNAP II and various transcription factors (TFs). Our further analysis revealed that not only rapid H2B turnover at cis-regulatory elements responses to heart disease, but also slow turnover at H3K27me3 sites functionally responses to heart disease with a different manner. More generally, we indicate that the binding and co-binding of DNA-binding proteins, such as TFs and epigenetic enzymes, all of them coupled with H2B turnover to modulate gene transcription and chromatin state.
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