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YTHDF1 functions as a non-canonical nuclear checkpoint that couples R-loop homeostasis to innate immune restraint and adaptive immune resistance in cancer（CUT&Tag）

ABSTRACT: Innate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling

ORGANISM(S): Homo sapiens

PROVIDER: GSE319911 | GEO | 2026/07/15

REPOSITORIES: GEO

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YTHDF1 functions as a non-canonical nuclear checkpoint that couples R-loop homeostasis to innate immune restraint and adaptive immune resistance in cancer（RNA-seq II）

Project description:Innate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling

2026-07-15 | GSE319703 | GEO

YTHDF1 functions as a non-canonical nuclear checkpoint that couples R-loop homeostasis to innate immune restraint and adaptive immune resistance in cancer（RNA-seq i）

2026-07-15 | GSE319690 | GEO

YTHDF1 functions as a non-canonical nuclear checkpoint that couples R-loop homeostasis to innate immune restraint and adaptive immune resistance in cancer（R-loop CUT&Tag）

2026-07-15 | GSE319910 | GEO

ARID1A regulates chromatin organization and establishment of epigenetic marks for DSB repair and transcription silencing

Project description:AT-rich interactive domain-containing protein 1A (ARID1A), a SWI/SNF chromatin remodeling complex subunit, is frequently mutated across various cancer entities. ARID1A contributes to DNA damage response pathways, and we previously reported that ARID1A loss is associated with mutational signatures linked to DNA repair defects. Here we show that ARID1A is promoting both DNA double-strand breaks (DSBs) repair pathways, non-homologous end-joining (NHEJ) and homologous recombination (HR). ARID1A is accumulated at DSBs after DNA damage and regulates the chromatin loop formation at DSB sites by interacting with the cohesin subunit RAD21 and CTCF insulator protein promoting their enrichment around the DSBs. Further analysis demonstrates that ARID1A’s involvement in DSB repair is accompanied by alterations of chromatin accessibility and distribution of activating histone marks at DSBs. ARID1A binds to and promotes the recruitment of the HDAC1 to control transcription repression at these DSBs. Altogether, ARID1A simultaneously regulates DSB repair and transcription silencing in transcriptionally active chromatin. ARID1A depletion resulted in defective DSB repair, which subsequently led to accumulation of micronuclei, activation of cGAS-STING pathway and an increased expression of immunomodulatory cytokines and chemokines upon IR treatment. Furthermore, low ARID1A expression in cancer patients receiving radiotherapy was associated with higher infiltration of several immune cells. The high mutation rate of ARID1A in various cancer types highlights its clinical relevance as a promising biomarker that correlates with the level of immune regulatory cytokines and can estimate the levels of tumor-infiltrating immune cells and response to combination of radio- and immunotherapy.

2025-04-08 | PXD046159 | Pride

ARID1A regulates chromatin organization and establishment of epigenetic marks for DSB repair and transcription silencing

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2024-01-15 | GSE211123 | GEO

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Project description:We performed CUT&Tag of inducible FOXD3 KO cells with or without cell cycle phase sorting to determine impact of FOXD3 loss of active chromatin marks.

2023-04-30 | GSE183419 | GEO

Comparative analyses of ChIP-seq, CUT&RUN and CUT&Tag for Polycomb chromatin profiling

Project description:Chromatin profiling methods such as ChIP-seq, CUT&RUN, and CUT&Tag differ substantially in background structure, signal distribution, and resolution, complicating direct quantitative comparison across platforms. In this study, we systematically compared conventional and double-crosslink ChIP-seq, CUT&RUN, and CUT&Tag by profiling the Polycomb-associated histone modification H3K27me3 in human cardiomyocytes and the PRC2 catalytic subunit EZH2 in pluripotent stem cells. To enable cross-assay comparison, we developed a biologically informed normalization strategy based on stable Polycomb reference loci, allowing harmonization of signal scales while preserving assay-intrinsic signal architecture. This approach revealed that CUT&RUN preferentially captures broad H3K27me3 domains, whereas CUT&Tag provides sharper and more localized enrichment for both H3K27me3 and EZH2. Together, our results establish a practical framework for cross-platform epigenomic comparison and guide the selection of chromatin profiling strategies. This GEO submission includes only datasets newly generated in this study. Additional publicly available datasets analyzed for comparison are cited in the associated manuscript and were not re-submitted here.

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