Telomerase function and binding at endogenous G-rich regions (Hi-C Seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA599165 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10834647_1.fastq.gz | Fastqsanger.gz | |||
| SRR10834647_2.fastq.gz | Fastqsanger.gz |
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Project description:Telomerase majorly functions at telomeres but under adverse conditions acts at endogenous regions, which is often observed in cancer calls. By mapping the global occupancy of the catalytic subunit of telomerase (Est2), we reveal that telomerase binds to multiple genomic loci, which we termed ‘non-telomere-binding sites’ (NTBS). We characterized under when and why Est2 binds to such sites and could show that telomerase is inactive but becomes activated upon global DNA damage. Indicating that those regions are of particular risk for genome stability. Using biochemical and molecular experiments we further characterized Est2 binding to NTBS. In contrast to Est2 binding to telomere neither Cdc13 nor Ku70/80 is crucial for the binding to NTBS. Strikingly, using Hi-C, we demonstrate that chromatin organization is essential and drives the interaction of Est2-NTBS binding. The here presented results provide a novel model of telomerase regulation using endogenous regions as “parking spots” awaiting its canonical function at telomeres.
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Project description:Telomerase function and binding at endogenous G-rich regions
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Project description:Telomerase majorly functions at telomeres but under adverse conditions acts at endogenous regions, which is often observed in cancer calls. By mapping the global occupancy of the catalytic subunit of telomerase (Est2), we reveal that telomerase binds to multiple genomic loci, which we termed ‘non-telomere-binding sites’ (NTBS). We characterized under when and why Est2 binds to such sites and could show that telomerase is inactive but becomes activated upon global DNA damage. Indicating that those regions are of particular risk for genome stability. Using biochemical and molecular experiments we further characterized Est2 binding to NTBS. In contrast to Est2 binding to telomere neither Cdc13 nor Ku70/80 is crucial for the binding to NTBS. Strikingly, using Hi-C, we demonstrate that chromatin organization is essential and drives the interaction of Est2-NTBS binding. The here presented results provide a novel model of telomerase regulation using endogenous regions as “parking spots” awaiting its canonical function at telomeres.
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Project description:Telomerase function and binding at endogenous G-rich regions (ChIP)
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Project description:Symmetrical dimethylation on arginine-3 of histone H4 (H4R3me2s) has been reported to occur at several repressed genes, but its specific regulation and genomic distribution remained unclear. Here, we show that the type-II protein arginine methyltransferase PRMT5 controls H4R3me2s in mouse embryonic fibroblasts (MEFs). In these differentiated cells, we find that the genome-wide pattern of H4R3me2s is highly similar to that in embryonic stem cells. In both the cell types, H4R3me2s peaks are detected predominantly at G + C-rich regions. Promoters are consistently marked by H4R3me2s, independently of transcriptional activity. Remarkably, H4R3me2s is mono-allelic at imprinting control regions (ICRs), at which it marks the same parental allele as H3K9me3, H4K20me3 and DNA methylation. These repressive chromatin modifications are regulated independently, however, since PRMT5-depletion in MEFs resulted in loss of H4R3me2s, without affecting H3K9me3, H4K20me3 or DNA methylation. Conversely, depletion of ESET (KMT1E) or SUV420H1/H2 (KMT5B/C) affected H3K9me3 and H4K20me3, respectively, without altering H4R3me2s at ICRs. Combined, our data indicate that PRMT5-mediated H4R3me2s uniquely marks the mammalian genome, mostly at G + C-rich regions, and independently from transcriptional activity or chromatin repression. Furthermore, comparative bioinformatics analyses suggest a putative role of PRMT5-mediated H4R3me2s in chromatin configuration in the nucleus. High throughput sequencing data from H4R3me2s native ChIP samples from mouse embryonic stem cells and fibroblasts were generated using Illumina Hi-seq 2000.
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