Cited by 280Genomics and Chromatin DynamicsChromosomal and Genetic VariationsEpigenetics and DNA Methylation

A heterochromatin-dependent transcription machinery drives piRNA expression

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Andersen, Peter Refsing, Tirian, Laszlo, Vunjak, Milica, Brennecke, Julius·2017·Nature

Abstract

Nuclear small RNA pathways safeguard genome integrity by establishing transcription-repressing heterochromatin at transposable elements. This inevitably also targets the transposon-rich source loci of the small RNAs themselves. How small RNA source loci are efficiently transcribed while transposon promoters are potently silenced is not understood. Here we show that, in Drosophila, transcription of PIWI-interacting RNA (piRNA) clusters-small RNA source loci in animal gonads-is enforced through RNA polymerase II pre-initiation complex formation within repressive heterochromatin. This is accomplished through Moonshiner, a paralogue of a basal transcription factor IIA (TFIIA) subunit, which is recruited to piRNA clusters via the heterochromatin protein-1 variant Rhino. Moonshiner triggers transcription initiation within piRNA clusters by recruiting the TATA-box binding protein (TBP)-related factor TRF2, an animal TFIID core variant. Thus, transcription of heterochromatic small RNA source loci relies on direct recruitment of the core transcriptional machinery to DNA via histone marks rather than sequence motifs, a concept that we argue is a recurring theme in evolution.

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  • Cells have two layers of defense against potentially deleterious transposable element activation: transcription is limited by heterochromatin-mediated silencing, and transcripts are cleared by piRNA-mediated degradation.

    “Based on current understanding, cells have two layers of defense against potentially deleterious transposable element activation: 1) Transposable element transcription is limited by heterochromatin-mediated silencing, and 2) Transposable element transcripts are cleared from the cell by piRNA-mediated degradation”

    From Pathogenic tau-induced piRNA depletion promotes neuronal death through transposable element dysregulation in neurodegenerative tauopathies (2018) · cites this paper as [39]

    The Abstract and Discussion (pages unavailable) support heterochromatin-mediated repression of transposon transcription. The Abstract also says the piRNA pathway targets transposons post-transcriptionally, but our copy does not specify that this clears their transcripts through degradation. (LLM, conf=0.83)

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  1. [75]Wickham H ggplot2 2016 Springer

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Authors
Andersen, P. R., Tirian, L., Vunjak, M., & Brennecke, J.
Affiliations
Institute of Molecular Biotechnology (AT)
Corresponding author
  • Andersen, Peter Refsing
  • Brennecke, Julius
Venue
Nature
Published
2017-08-23
Volume
549
Issue
7670
Pages
54-59
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2748864067
Cited by
280
References
78
Citations by year
2026: 20 · 2025: 32 · 2024: 39 · 2023: 37 · 2022: 21 · 2021: 35 · 2020: 25 · 2019: 37 · 2018: 27 · 2017: 6 · 2016: 1
FWCI
10.62
Type
journal article
Language
en
Open access
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
Novo Nordisk Fonden (NNF14OC0009189)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
piRNA, heterochromatin, rhinoceros, HP1, TRF2, TFIID, transposon silencing, germline, Drosophila, histone modifications, genome stability
MeSH terms
Animals, Chromosomal Proteins, Non-Histone, DNA Transposable Elements, Drosophila melanogaster, Female, Multigene Family, Heterochromatin, Promoter Regions, Genetic, RNA Polymerase II, Transcription, Genetic, Gene Silencing, Drosophila Proteins, RNA, Small Interfering, Telomeric Repeat Binding Protein 2, Transcription Factor TFIIA, Transcription Initiation, Genetic

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