Mapping PT modifications in bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA560558 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9988660_1.fastq.gz | Fastqsanger.gz | |||
| SRR9988660_2.fastq.gz | Fastqsanger.gz | |||
| SRR9988661_1.fastq.gz | Fastqsanger.gz | |||
| SRR9988661_2.fastq.gz | Fastqsanger.gz | |||
| SRR9988662_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:One microbial organism always contains multiple DNA modification systems as defense strategies or epigenetic controls. Here, we describe crosstalk between two distinct DNA modifications with different target sequence motif: DNA phosphorothioation (PT, GPSAAC/GPSTTC by DndACDE proteins) and N6-methyl-adenine methylation (m6A, G6mATC by Dam protein). By using a newly developed DNA modification sequencing method PT nick-seq, we found that half of PT modifications change from GAAC/GTTC to GATC sites after bacteria have lost Dam.
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Project description:Endogenous and exogenous chemical modifications in DNA have profound influences on genome function. We have developed a novel technology, Nick-seq, for mapping variety of DNA chemical modifications across the genomes at single-nucleotide resolution, by which we achieved quantitative profiling of single-strand breaks, phosphorothioate modifications, and oxidative DNA damage sites. This method is applicable for mapping of any DNA metabolism events that are involved in or can be converted, enzymatically or chemically, to DNA strand breaks such as DNA modifications, damages, genome replication, and chromatin structures.
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Project description:Platinum-based drugs (Pt drugs) are widely used in cancer chemotherapy, yet their genome-wide DNA binding patterns remain incompletely understood. Here, we present Pt-seq, an antibody-assisted, genome-wide method for mapping Pt-DNA adducts at single-base resolution. By employing exo- and endo- nucleases to remove background DNA, Pt-seq enables highly robust and sensitive profiling of binding sites for cisplatin, oxaliplatin, lobaplatin, and a Pt(IV) complex. Using Pt-seq, we identified hundreds to a few thousand binding clusters that are 10-20 kb in length and highly consistent among different Pt drugs. Notably, these binding clusters predominantly localize to centromeric and rDNA regions. In cisplatin-resistant cells, we found significantly reduced binding within these regions, suggesting a potential role in drug resistance. Moreover, we found that de novo mutations in cancer cells can create novel binding sites for Pt drugs. Based on this, we demonstrated that ICR-191, an acridine orange compound capable of inducing G insertions, enhances cisplatin-DNA crosslinking and sensitizes cells to Pt drugs. Collectively, Pt-seq sensitively profiles Pt drug-DNA interactions and deepens our understanding of the genome-wide effect of chemotherapeutic drugs.
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Project description:Platinum-based drugs (Pt drugs) are widely used in cancer chemotherapy, yet their genome-wide DNA binding patterns remain incompletely understood. Here, we present Pt-seq, an antibody-assisted, genome-wide method for mapping Pt-DNA adducts at single-base resolution. By employing exo- and endo- nucleases to remove background DNA, Pt-seq enables highly robust and sensitive profiling of binding sites for cisplatin, oxaliplatin, lobaplatin, and a Pt(IV) complex. Using Pt-seq, we identified hundreds to a few thousand binding clusters that are 10-20 kb in length and highly consistent among different Pt drugs. Notably, these binding clusters predominantly localize to centromeric and rDNA regions. In cisplatin-resistant cells, we found significantly reduced binding within these regions, suggesting a potential role in drug resistance. Moreover, we found that de novo mutations in cancer cells can create novel binding sites for Pt drugs. Based on this, we demonstrated that ICR-191, an acridine orange compound capable of inducing G insertions, enhances cisplatin-DNA crosslinking and sensitizes cells to Pt drugs. Collectively, Pt-seq sensitively profiles Pt drug-DNA interactions and deepens our understanding of the genome-wide effect of chemotherapeutic drugs.
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Project description:Pt-ttpy (tolyl terpyridin-Pt complex) covalently binds to G-quadruplex (G4) structures in vitro and to telomeres in cellulo via its Pt moiety. Here, we identified its targets in the human genome, in comparison to Pt-tpy, its derivative without G4 affinity, and cisplatin. Pt-ttpy, but not Pt-tpy, induces the release of the shelterin protein TRF2 from telomeres concomitantly to the formation of DNA damage foci at telomeres but also at other chromosomal locations. -H2AX chromatin immunoprecipitation (ChIP-seq) after treatment with Pt-ttpy or cisplatin revealed accumulation in G- and A-rich tandemly repeated sequences, but not particularly in potential G4 forming sequences. Collectively, Pt-ttpy presents dual targeting efficiency on DNA, by inducing telomere dysfunction and genomic DNA damage at specific loci.
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