Dataset Information

ChAHP Silences SINE Retrotransposons by Inhibiting TFIIIB Recruitment

ABSTRACT: Short interspersed nuclear elements (SINEs) are abundant non-autonomous transposable elements derived from RNA polymerase III (Pol III)-transcribed short non-coding RNAs. SINEs retain sequence features recognized by the Pol III machinery and constitute a substantial portion of vertebrate genomes. Despite their impact on genome stability and evolution, the mechanisms governing SINE transcription remain poorly understood. Although DNA methylation and heterochromatin formation have been implicated in their repression, we find these pathways play only a minor role in mouse embryonic stem cells. Instead, we identify the ChAHP complex as a key repressor of SINE B2 elements. ChAHP directly inhibits Pol III transcription by blocking TFIIIB recruitment without affecting TFIIIC binding. This selective interference prevents transcription initiation and highlights a distinct regulatory mechanism. Our findings establish ChAHP as a non-canonical repressor of Pol III-dependent SINE transcription, offering new insights into the control of this pervasive class of non-coding genomic elements.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Embryonic Stem Cell

SUBMITTER: Jan Seebacher

LAB HEAD: Marc Buehler

PROVIDER: PXD064515 | Pride | 2026-06-30

REPOSITORIES: Pride

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			Action	DRS
	L2_220615_DH_3195_Ctrl2_S04.raw	Raw
	L2_220615_DH_3195_Ctrl2_S05.raw	Raw
	L2_220615_DH_3195_Ctrl2_S06.raw	Raw
	L2_220615_DH_3195_Gtf3c1_S10.raw	Raw
	L2_220615_DH_3195_Gtf3c1_S11.raw	Raw

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Project description:The cellular accumulation of short non-coding RNAs (ncRNAs) transcribed by RNA Polymerase III (Pol III) is a hallmark of various cellular stressors and inflammatory-associated diseases. Yet, the mechanisms driving the accumulation of these RNAs are largely undefined. Infection with several DNA viruses is known to significantly alter the cellular Pol III transcriptome, leading to the induction of a class of non-coding retrotransposons known as short interspersed nuclear elements (SINE) and tRNA genes. Here, we sought to define the mechanisms driving Pol III transcribed ncRNA abundance during viral infection, using the murine herpesvirus MHV68 as a model. Our findings reveal that while the expression of Pol III transcripts, such as the murine-specific family of B2 SINE ncRNAs and pre-tRNAs, significantly increase during MHV68 infection, Pol III genomic occupancy is enhanced at a much fewer subset of B2 SINE and tRNA genes. Using DNA motif analyses and a convolutional neural network (CNN) based model, we identified non-promoter sequence elements within B2 SINE genes that distinguish infection-induced loci. We found that infection-induced B2 SINE genes are enriched for signal sequences that confer polyadenylation, and endogenous B2 SINE ncRNA polyadenylation depends on mRNA cleavage and polyadenylation (CPSF) machinery. We discovered that mRNA CPSF components are recruited to sites of Pol III transcription in response to MHV68 infection in a manner dependent on Pol III occupancy. Chromatin-associated B2 SINE ncRNAs are also bound by the CPSF complex, suggesting an RNA-dependent, co-transcriptional polyadenylation of B2 SINE ncRNAs. This uncovers an inducible, coupled relationship between Pol III transcription and mRNA-like polyadenylation of ncRNAs. Also, CPSF recruitment to Pol III genes is not restricted to murine genomes but also occurs at human SINE and tRNA genes, suggesting that this previously unknown coupled relationship may be a widespread feature of Pol III transcription.

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ChAHP Silences SINE Retrotransposons by Inhibiting TFIIIB Recruitment

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