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PhpCNF-Y transcription factor infiltrates heterochromatin to generate cryptic intron-containing transcripts crucial for small RNA production [Small RNA-Seq]

ABSTRACT: The assembly of repressive heterochromatin in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA-based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeats are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) PhpCNF-Y complex can infiltrate constitutive heterochromatin via its histone-fold domains to transcribe repeat elements. PhpCNF-Y collaborates with a Zn-finger containing TF to bind repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, PhpCNF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain multiple cryptic introns whose predicted splice sites are required for the generation of small interfering RNAs (siRNAs) via a mechanism requiring the spliceosome. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for heterochromatin nucleation at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE279535 | GEO | 2025/10/15

REPOSITORIES: GEO

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PhpNF-Y transcription factor infiltrates repressive heterochromatin to generate transcripts crucial for spliceosome-dependent small RNA production

Project description:The assembly of repressive heterochromatin domains in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA-based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeat elements are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) PhpCNF-Y complex, which includes histone fold domain proteins, can infiltrate constitutive heterochromatin to transcribe repeat elements. PhpCNF-Y collaborates with a Zn-finger containing TF to bind heterochromatic repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, PhpCNF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain cryptic introns that are processed via a mechanism requiring the spliceosome to generate small interfering RNAs (siRNAs) by the RNAi machinery. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for nucleation of heterochromatin at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.

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PhpCNF-Y transcription factor infiltrates heterochromatin to generate cryptic intron-containing transcripts crucial for small RNA production [ChIP-Seq]

Project description:The assembly of repressive heterochromatin in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA-based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeats are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) PhpCNF-Y complex can infiltrate constitutive heterochromatin via its histone-fold domains to transcribe repeat elements. PhpCNF-Y collaborates with a Zn-finger containing TF to bind repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, PhpCNF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain multiple cryptic introns whose predicted splice sites are required for the generation of small interfering RNAs (siRNAs) via a mechanism requiring the spliceosome. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for heterochromatin nucleation at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.

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Project description:The assembly of repressive heterochromatin in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA- based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeats are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) Php|NF-Y complex, which includes histone fold domain proteins, can infiltrate constitutive heterochromatin to transcribe repeat elements. Php|NF-Y collaborates with a Zn-finger containing TF to bind repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, Php|NF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain cryptic introns that are processed via a mechanism requiring the spliceosome to generate small interfering RNAs (siRNAs) by the RNAi machinery. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for heterochromatin nucleation at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.

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Project description:Heterochromatin regions of the genome are transcriptionally repressive in nature. However, constitutive heterochromatin, such as at centromeres and telomeres, coats regions harboring multiple repetitive DNA elements that are preferentially transcribed during S-phase by RNA polymerase II. RNAi machinery processes the transcripts to generate small RNAs (siRNAs) that are crucial for heterochromatin assembly. Despite significant mechanistic advances in the field, the contribution of transcription factor (TF) based mechanisms to repeat element transcription and siRNA production is unclear. Here, we discover that the conserved TF PhpCNF-Y, which contains a histone fold motif, collaborates with a Zn-finger domain-containing factor, Moc3, to access specific sites within the heterochromatin region, regardless of the presence of the repressive histone methylation mark. The cooperative function of the TFs is essential for gaining access to the heterochromatin region, where they bind to specific CCAAT motif sites within the heterochromatic repeat elements cenH and dh. Perturbation of heterochromatin has minimal effect on the binding of the TFs to these specific sites, and they remain bound even outside of the S-phase. We find that PhpCNF-Y and Moc3 mediate the transcription of the repeat elements originating from a bottom strand of cenH, which the spliceosome targets to generate siRNAs in a Swi6HP1-independent manner. This pathway for generating the initial transcripts is crucial for de novo heterochromatin assembly. Collectively, our study uncovers a fundamental transcription factor-based mechanism that gains access to the heterochromatin to enforce transcriptional silencing of repeat elements. Our findings provide significant insights into de novo heterochromatin assembly.

2025-10-15 | GSE279525 | GEO

PhpNF-Y drives heterochromatic transcription to generate splicing machinery-dependent small RNAs (RNA-Seq)

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PhpNF-Y drives heterochromatic transcription to generate splicing machinery-dependent small RNAs (ChIP-Seq)

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2023-05-26 | PXD028824 | Pride

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