ChAHP Displaces Transcriptional Regulators Through Active Chromatin Remodeling
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ABSTRACT:
PROVIDER: PRJNA1266616 | ENA |
REPOSITORIES: ENA
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Project description:ChAHP Displaces Transcriptional Regulators Through Active Chromatin Remodeling [gNOMEseq]
| PRJNA1266605 | ENA
Project description:ChAHP Displaces Transcriptional Regulators Through Active Chromatin Remodeling [RNAseq]
| PRJNA1266618 | ENA
Project description:ChAHP Displaces Transcriptional Regulators Through Active Chromatin Remodeling [ChIPseq]
| PRJNA1266620 | ENA
Project description:Transcriptional control in eukaryotes relies on the coordinated action of chromatin-based regulatory mechanisms, including control of nucleosome occupancy and chromatin modifications. We previously identified the ChAHP complex – comprising the chromatin remodeler CHD4, transcription factor ADNP, and HP1 proteins – as a repressor of SINE B2 retrotransposons and site-specific regulator of CTCF engagement with chromatin. However, the molecular basis of these functions remained unresolved. Here, we show that ChAHP-associated CHD4 is essential for SINE B2 repression, while HP1 proteins are dispensable. We further demonstrate that CHD4’s remodeling activity is not required for chromatin binding, but is critical for both retrotransposon silencing and efficient CTCF antagonism. We propose ChAHP is a sequence-specific recruiter of chromatin remodeling activity, facilitating transcriptional control and localized modulation of chromatin architecture.
2025-07-21 | GSE297862 | GEO
Project description:Transcriptional control in eukaryotes relies on the coordinated action of chromatin-based regulatory mechanisms, including control of nucleosome occupancy and chromatin modifications. We previously identified the ChAHP complex – comprising the chromatin remodeler CHD4, transcription factor ADNP, and HP1 proteins – as a repressor of SINE B2 retrotransposons and site-specific regulator of CTCF engagement with chromatin. However, the molecular basis of these functions remained unresolved. Here, we show that ChAHP-associated CHD4 is essential for SINE B2 repression, while HP1 proteins are dispensable. We further demonstrate that CHD4’s remodeling activity is not required for chromatin binding, but is critical for both retrotransposon silencing and efficient CTCF antagonism. We propose ChAHP is a sequence-specific recruiter of chromatin remodeling activity, facilitating transcriptional control and localized modulation of chromatin architecture.
2025-07-21 | GSE297861 | GEO
Project description:Transcriptional control in eukaryotes relies on the coordinated action of chromatin-based regulatory mechanisms, including control of nucleosome occupancy and chromatin modifications. We previously identified the ChAHP complex – comprising the chromatin remodeler CHD4, transcription factor ADNP, and HP1 proteins – as a repressor of SINE B2 retrotransposons and site-specific regulator of CTCF engagement with chromatin. However, the molecular basis of these functions remained unresolved. Here, we show that ChAHP-associated CHD4 is essential for SINE B2 repression, while HP1 proteins are dispensable. We further demonstrate that CHD4’s remodeling activity is not required for chromatin binding, but is critical for both retrotransposon silencing and efficient CTCF antagonism. We propose ChAHP is a sequence-specific recruiter of chromatin remodeling activity, facilitating transcriptional control and localized modulation of chromatin architecture.
2025-07-21 | GSE297860 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-07-21 | GSE297864 | GEO
Project description:Retrotransposon control in mammals is an intricate process that is effectuated by a broad network of chromatin regulatory pathways. We previously discovered ChAHP, a protein complex with repressive activity against SINE retrotransposons, composed of the transcription factor ADNP, chromatin remodeler CHD4, and HP1 proteins. Here we identify ChAHP2, a protein complex homologous to ChAHP, wherein ADNP is replaced by ADNP2. ChAHP2 is predominantly targeted to ERVs and LINEs, via HP1b-mediated binding of H3K9 trimethylated histones. We further demonstrate that ChAHP also binds these elements in a mechanistically equivalent manner to ChAHP2, and distinct from DNA sequence-specific recruitment at SINEs. Genetic ablation of ADNP2 alleviates ERV and LINE1 repression, which is synthetically exacerbated by additional depletion of ADNP. Together, our results reveal that the ChAHP and ChAHP2 complexes function to control both non-autonomous and autonomous retrotransposons by complementary activities, further adding to the complexity of mammalian transposon control.
2024-06-25 | GSE253067 | GEO
Project description:Retrotransposon control in mammals is an intricate process that is effectuated by a broad network of chromatin regulatory pathways. We previously discovered ChAHP, a protein complex with repressive activity against SINE retrotransposons, composed of the transcription factor ADNP, chromatin remodeler CHD4, and HP1 proteins. Here we identify ChAHP2, a protein complex homologous to ChAHP, wherein ADNP is replaced by ADNP2. ChAHP2 is predominantly targeted to ERVs and LINEs, via HP1b-mediated binding of H3K9 trimethylated histones. We further demonstrate that ChAHP also binds these elements in a mechanistically equivalent manner to ChAHP2, and distinct from DNA sequence-specific recruitment at SINEs. Genetic ablation of ADNP2 alleviates ERV and LINE1 repression, which is synthetically exacerbated by additional depletion of ADNP. Together, our results reveal that the ChAHP and ChAHP2 complexes function to control both non-autonomous and autonomous retrotransposons by complementary activities, further adding to the complexity of mammalian transposon control.
2024-06-25 | GSE253066 | GEO
Project description:Retrotransposon control in mammals is an intricate process that is effectuated by a broad network of chromatin regulatory pathways. We previously discovered ChAHP, a protein complex with repressive activity against SINE retrotransposons, composed of the transcription factor ADNP, chromatin remodeler CHD4, and HP1 proteins. Here we identify ChAHP2, a protein complex homologous to ChAHP, wherein ADNP is replaced by ADNP2. ChAHP2 is predominantly targeted to ERVs and LINEs, via HP1b-mediated binding of H3K9 trimethylated histones. We further demonstrate that ChAHP also binds these elements in a mechanistically equivalent manner to ChAHP2, and distinct from DNA sequence-specific recruitment at SINEs. Genetic ablation of ADNP2 alleviates ERV and LINE1 repression, which is synthetically exacerbated by additional depletion of ADNP. Together, our results reveal that the ChAHP and ChAHP2 complexes function to control both non-autonomous and autonomous retrotransposons by complementary activities, further adding to the complexity of mammalian transposon control.
2024-06-25 | GSE253065 | GEO