Silencio/CG9754 connects the Piwi-piRNA complex to the cellular heterochromatin machinery
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The repression of transposable elements in eukaryotes often involves their transcriptional silencing via targeted chromatin modifications. In animal gonads, nuclear Argonaute proteins of the PIWI clade complexed with small guide RNAs (piRNAs) serve as sequence specificity determinants in this process. How binding of nuclear PIWI–piRNA complexes to nascent transcripts orchestrates heterochromatin formation and transcriptional silencing is unknown. Here, we characterize CG9754/Silencio as an essential piRNA pathway factor that is required for Piwi-mediated transcriptional silencing in Drosophila. Ectopic targeting of Silencio to RNA or DNA is sufficient to elicit silencing independently of Piwi and known piRNA pathway factors. Instead, Silencio requires the H3K9 methyltransferase Eggless/SetDB1 for its silencing ability. In agreement with this, SetDB1, but not Su(var)3-9, is required for Piwi-mediated transcriptional silencing genome-wide. Due to its interaction with the target-engaged Piwi–piRNA complex, we suggest that Silencio acts as linker between the sequence specificity factor Piwi and the cellular heterochromatin machinery.
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Egg is involved in de novo H3K9me3 establishment, while Su(var)3-9 is required for H3K9me3 spreading.
“which may be due to the fact that Egg is involved in de novo H3K9me3 establishment, while Su(var)3–9 is required for H3K9me3 spreading (84)”
From Impaired function of rDNA transcription initiation machinery leads to derepression of ribosomal genes with insertions of R2 retrotransposon (2022) · cites this paper as [84]
The Results section, “Distinct roles of SetDB1 and Su(var)3-9 at piRNA targeted TE insertions,” proposes that Egg/SetDB1 initiates heterochromatin formation and Su(var)3-9 assists H3K9me3 spreading at piRNA-targeted TE insertions. It reports reduced, not abolished, spreading after Su(var)3-9 depletion. The claim’s unqualified statement that Su(var)3-9 is required for spreading is stronger and broader than the paper’s finding. (LLM, conf=0.85)
Experimental — accuracy not yet measuredEgg knockdown causes about a 40-fold derepression of the telomeric HeT-A element.
“Note that Egg was previously shown to be strongly required for transcriptional silencing of a broad range of TEs in ovaries (84) and its knockdown caused about a 40-fold derepression of telomeric HeT-A element in our analysis (Figure 2A).”
From Impaired function of rDNA transcription initiation machinery leads to derepression of ribosomal genes with insertions of R2 retrotransposon (2022) · cites this paper as [84]
Germline knockdown of Su(var)3-9 leads to much more severe oogenesis defects than Egg depletion but also induces a 2-3-fold upregulation of R1 and R2 elements.
“GKD of another HMT, Su(var)3–9 known to be involved in the formation of constitutive heterochromatin and the spreading of the H3K9me3 mark (84–86) led to much more severe defects of oogenesis than Egg depletion but also induced a 2–3-fold upregulation of R1 and R2 elements (Figure 2A).”
From Impaired function of rDNA transcription initiation machinery leads to derepression of ribosomal genes with insertions of R2 retrotransposon (2022) · cites this paper as [84]
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Silencing transposable elements in the Drosophila germline
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Piwi–piRNA complexes induce stepwise changes in nuclear architecture at target loci
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“Note that Egg was previously shown to be strongly required for transcriptional silencing of a broad range of TEs in ovaries (84) and its knockdown caused about a 40fold derepression of telomeric HeT-A element in our analysis (Figure 2A).”
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Maternally inherited siRNAs initiate piRNA cluster formationPreprint
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- Authors
- Sienski, G., Batki, J., Senti, K.-A., Dönertas, D., Tirian, L., Meixner, K., & Brennecke, J.
- Affiliations
- Institute of Molecular Biotechnology (AT)
- Corresponding author
- Brennecke, Julius
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2015-10-22
- Volume
- 29
- Issue
- 21
- Pages
- 2258-2271
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC4647559
- OpenAlex
- W2158625565
- Cited by
- 185
- References
- 67
- Citations by year
- 2026: 8 · 2025: 23 · 2024: 13 · 2023: 11 · 2022: 12 · 2021: 20 · 2020: 22 · 2019: 20 · 2018: 27 · 2017: 13 · 2016: 16
- Type
- posted content
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Genes & Development (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Austrian Academy of Sciences
- European Community's 7th Framework Programme (260711EU)
- Austrian Science Fund (Y 510-B12, F4303-B09, W12-7-B09)
- Boehringer Ingelheim
- European Union (FP7-MC-IEF-253912)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- transposon silencing, transcriptional silencing, heterochromatin formation, H3K9 methyltransferase, SETDB1, Su(var)3-9, piRNA pathway, Drosophila, chromatin modification
- MeSH terms
- Animals, DNA, DNA Transposable Elements, Drosophila melanogaster, Female, Heterochromatin, Histones, Methylation, Nuclear Proteins, Ovary, Protein Binding, Histone-Lysine N-Methyltransferase, Repressor Proteins, RNA, RNA-Binding Proteins, Gene Expression Regulation, Developmental, Gene Silencing, Drosophila Proteins, RNA, Small Interfering, Genome, Insect, Argonaute Proteins
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