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PURPL plays a role in epigenetic regulation of gene expression [ChIP-Seq]

ABSTRACT: Cellular senescence involves heterochromatin reorganization and aberrant gene expression. We demonstrate that the nuclear-enriched lncRNA PURPL regulates senescence-associated chromatin dynamics by modulating H3K9me3 deposition. PURPL knockdown increased global H3K9me3 levels while its overexpression reduced this repressive mark. Genome-wide analysis revealed 411 loci with PURPL-dependent H3K9me3 changes, including the aging-related gene SERPINE1, where H3K9me3 accumulation correlated with transcriptional repression. These findings establish PURPL as an epigenetic regulator of senescence through targeted control of heterochromatin formation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301169 | GEO | 2025/12/02

REPOSITORIES: GEO

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Targeting PURPL RNA Enabled Rejuvenation of Senescence Cells via Epigenetic Reprogramming

Project description:Cellular senescence is a fundamental driver of ageing and age-related diseases, characterized by irreversible growth arrest and profound epigenetic alterations. While long non-coding RNAs (lncRNAs) have emerged as key regulators of senescence, their potential for senescent cell rejuvenation remains unexplored. Here, we identify the ageing-associated lncRNA PURPL as an epigenetic regulator that controls cellular rejuvenation through H3K9me3-mediated transcriptional silencing. CRISPRi-mediated PURPL depletion produces striking rejuvenation effects, resulting in restored youthful cell morphology, as well as suppression of senescence markers such as p21 and SA-β-gal. Conversely, PURPL overexpression accelerates cellular senescence, recapitulating the transcriptional and phenotypic hallmarks of ageing. Mechanistically, nuclear-localized PURPL regulates H3K9me3 deposition at 411 genomic loci including SERPINE1 (PAI-1) and EGR1, which are key senescence drivers. PURPL-mediated H3K9me3 loss at these loci derepresses their transcription, establishing a pro-senescence gene expression program. These findings reveal that PURPL is an epigenetic modulator of senescence and highlight its potential as a therapeutic target for age-related pathologies.

2025-10-27 | PXD068664 | Pride

PURPL bidirectionally controls senescence: depletion rejuvenates fibroblasts while overexpression accelerates aging [RNA-Seq2]

Project description:ellular senescence is a fundamental driver of aging and age-related diseases, with long non-coding RNAs (lncRNAs) emerging as critical regulators of this process. Here, we identify PURPL as a bidirectional modulator of senescence in human fibroblasts. Through comparative transcriptomic analysis of replicative and doxorubicin-induced senescence models, we discovered PURPL as the most significantly upregulated lncRNA common to both systems. CRISPR interference (CRISPRi)-mediated PURPL depletion in senescent cells reversed hallmark aging phenotypes, including restoration of LMNB1 expression, suppression of p21, and reduced SA-β-gal activity. Conversely, PURPL overexpression in young fibroblasts recapitulated senescence signatures, inducing extracellular matrix reorganization and cell cycle arrest pathways. RNA-seq revealed PURPL overexpression dysregulated 1,633 genes, mirroring natural aging transcriptomes. These opposing effects establish PURPL as a central regulator of cellular senescence, suggesting its therapeutic potential for age-related conditions. Our findings provide mechanistic insights into lncRNA-mediated senescence control and highlight PURPL as a novel target for aging intervention strategies.

2025-12-02 | GSE301166 | GEO

Identification of PURPL regulated genes in HCT116 cells

Project description:Analysis of changes in gene expression profile upon depletion of PURPL in HCT116 cells. The hypothesis in this study is that PURPL regulates gene expression in the p53 pathway.

2017-08-03 | GSE79053 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (Iso-Seq)

Project description:The goal of our study is to investigate the role of the p53-induced lncRNA PURPL in the context of liver cancer. To achieve this, we identified transcript variants of PURPL expressed in liver cancer cells and assayed for the transcriptome changes caused by PURPL knockdown after p53 induction.

2022-10-18 | GSE206701 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq II)

2022-10-18 | GSE206699 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq I)

2022-10-18 | GSE206698 | GEO

The loss of heterochromatin is associated with multiscale three-dimensional genome reorganization and aberrant transcription during cellular senescence

Project description:Heterochromatin remodeling is critical for various cell processes. In particular, the “loss of heterochromatin” phenotype in cellular senescence engages with the progress of aging and age-related disorders. Although biological processes of senescent cells including senescence-associated heterochromatin foci (SAHF) formation, chromosome compaction and entry into senescence have been closely associated with high-order chromatin structure. the relationship between the high-order chromatin organization and the loss of heterochromatin phenotype during senescence has not been fully understood. By using senescent and late senescent fibroblasts induced by DNA damage harboring the “loss of heterochromatin” phenotype, we observed progressive 3D reorganization of heterochromatin during senescence. Facultative and constitutive heterochromatin marked by H3K27me3 and H3K9me3, respectively, showed different alterations. Facultative heterochromatin tends to switch from the repressive B-compartment to the active A-compartment, whereas constitutive heterochromatin shows no significant changes at the compartment level but enhanced interactions between themselves. Interestingly, both types show increased chromatin accessibility and gene expression leakage during senescence. Furthermore, increased chromatin accessibility in potential CTCF binding sites accompanies by the establishment of novel loops in constitutive heterochromatin. Finally, we also observed aberrant expression of repetitive elements, including LTR (long terminal repeat) and satellite classes. Overall, facultative and constitutive heterochromatin show multiscale but distinct alterations in the 3D map, meanwhile they also share the same features of increased chromatin accessibility and gene expression leakage. This study provides an epigenomic map of heterochromatin reorganization during senescence.

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Mass spectrometry (MS) datasets of PURPL RNA pulldown samples in A375 cells

Project description:We performed PURPL RNA pulldown followed by MS analysis to identify purpl-interacting proteins in A375 cells.With high performance liquid chromatography-mass spectrometry (HPLC-MS), the binding protein of PURPL from RNA pull down was detected by removing non-specific protein which were binding with EGFP.

2022-02-16 | PXD028863 | Pride

PURPL Represses Radiation-induced Apoptosis to Promote Radioresistance in Cutaneous Melanoma by Direct Interfering with BID Cleavage

Project description:During the treatment of cutaneous melanoma, the presence of radioresistance compromised the therapeutic effects of radiotherapy. Yet, the mechanism of radioresistance in melanoma still remains unclear. Bioinformatic analysis of the transcriptomic sequencing showed PURPL was top up-regulated genes in response to ionizing radiation (IR) treatment in melanoma cells. Loss of PURPL notably repressed melanoma cell viability, colony formation, migration and invasiveness which potentiated PURPL’s role in radioresistance of melanoma. Further, loss-of- and gain-of-function analysis indicated that PURPL repressed IR-induced DNA damage and apoptosis. Mechanistically, RNA pulldown was performed and BID was identified as the interacting protein partner of PURPL. As the core gene of the mitochondrial apoptosis pathway, BID could be cleaved by Caspase-8 to generate tBID, which promotes the permeability of the mitochondrial membrane and the release of cytochrome c. IR treatment promotes the interaction between BID and Caspase-8 which was further strengthened by the loss of PURPL. The in vivo assays further verified the in vitro findings. Collectively, our study supports the pro-radioresistance role of PURPL in melanoma by inhibiting the interaction between BID and Caspase-8, which may provide a novel target for clinical radiotherapy.

2024-01-01 | GSE248024 | GEO

SMARCAD1 and TOPBP1 contribute to heterochromatin maintenance at the transition from the 2C-like to the pluripotent state

Project description:Chromocenters are established after the 2-cell (2C) stage during mouse embryonic development, but the factors that mediate chromocenter formation remain largely unknown. To identify regulators of 2C heterochromatin establishment, we generated an inducible system to convert embryonic stem cells (ESCs) to 2C-like cells. This conversion is marked by a global reorganization and dispersion of H3K9me3-heterochromatin foci, which are then reversibly formed upon re-entry into pluripotency. Profiling the chromatin-bound proteome (chromatome) by genome capture of ESCs transitioning to 2C-like cells, we uncover chromatin regulators involved in de novo heterochromatin formation. We identified TOPBP1 and investigated its binding partner SMARCAD1. SMARCAD1 and TOPBP1 associate with H3K9me3-heterochromatin in ESCs. Interestingly, the nuclear localization of SMARCAD1 is lost in 2C-like cells. SMARCAD1 or TOPBP1 depletion in mouse embryos lead to developmental arrest, reduction of H3K9me3 and remodeling of heterochromatin foci. Collectively, our findings contribute to comprehending the maintenance of chromocenters during early development.

2023-04-18 | PXD019703 | Pride

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