ArticleNucleic acids research2025
A specialized TFIIB is required for transcription of transposon-targeting noncoding RNAs.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- Transposon targeting non-coding RNA transcription targets G/C-rich tracts and is facilitated by an intrinsically disordered protein in Tetrahymena.Science China. Life sciences · 2026Article
- Ciliates: a window into the diversity and complexity of unicellular eukaryotic life.Science China. Life sciences · 2026Article
- Specific tracking of N-terminal clipping on histone H3 inMarine life science & technology · 2026Article
- Bromodomain protein IBD1 bridges histone acetylation and H2A.Z deposition to fine-tune transcription.Nucleic acids research · 2026Article
- Review
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Authors and funding
11 authors.
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Abstract
Transposable elements (TEs) pose threats to genome stability. Therefore, small RNA-mediated heterochromatinization suppresses the transcription and hence the mobility of TEs. Paradoxically, transcription of noncoding RNA (ncRNA) from TEs is needed for the production of TE-targeting small RNAs and/or recruiting the silencing machinery to TEs. Hence, specialized RNA polymerase II (Pol II) regulators are required for such unconventional transcription in different organisms, including the developmental stage-specific Mediator complex (Med)-associated proteins in the ncRNA transcription from TE-related sequences in Tetrahymena. Yet it remains unclear how the Pol II transcriptional machinery is assembled at TE-related sequences for the ncRNA transcription. Here, we report that Pol II is regulated by Emit3, a stage-specific TFIIB-like protein specialized in TE transcription. Emit3 interacts with the TFIIH complex and localizes to TE-dense regions, especially at sites enriched with a G-rich sequence motif. Deletion of Emit3 globally abolishes Pol II-chromatin association in the meiotic nucleus, disrupts the chromatin binding of Med, and impairs the TE-biased localization of TFIIH. Conversely, Emit3's preferential localization to TE-rich loci relies in part on Med-associated proteins. These findings suggest that Emit3, TFIIH, and Med-associated proteins work together to initiate Pol II ncRNA transcription from TE-dense regions, possibly in a sequence-dependent manner.
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