Ontology highlight
ABSTRACT:
PROVIDER: PRJNA515080 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8441390_1.fastq.gz | Fastqsanger.gz | |||
| SRR8441390_2.fastq.gz | Fastqsanger.gz | |||
| SRR8441381_1.fastq.gz | Fastqsanger.gz | |||
| SRR8441381_2.fastq.gz | Fastqsanger.gz | |||
| SRR8441391_1.fastq.gz | Fastqsanger.gz |
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Project description:Exploiting evolutionary steering to induce collateral drug sensitivity in cancer
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Project description:Chemotherapy resistance is a major obstacle to curing cancer patients. Combination drug regimens have shown promise as a method to overcome resistance; however, to date only some cancers have been cured with this method. Collateral sensitivity – the phenomenon whereby resistance to one drug is co-occurrent with sensitivity to a second drug – has been gaining traction as a promising new concept to guide rational design of combination regimens. Here we evolved over 100 subclones of the Eµ-Myc; p19ARF -/- cell line to be resistant to one of four classical chemotherapy agents: doxorubicin, vincristine, paclitaxel, and cisplatin. We then surveyed collateral responses to acquisition of resistance to these agents. Although numerous collateral sensitivities have been documented for antibiotics and targeted cancer therapies, we observed only one collateral sensitivity: half of cell lines that acquired resistance to paclitaxel also acquired a collateral sensitivity to verapamil. However, we found that the mechanism of this collateral sensitivity was unrelated to the mechanism of paclitaxel resistance. Interestingly, we observed heterogeneity in the phenotypic response to acquisition of resistance to most of the drugs we tested, most notably for paclitaxel, suggesting the existence of multiple different states of resistance. Surprisingly, this phenotypic heterogeneity in paclitaxel resistant cell lines was unrelated to transcriptomic heterogeneity among those cell lines. These features of phenotypic and transcriptomic heterogeneity must be taken into account in future studies of treated tumor subclones and in design of chemotherapy combinations.
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Project description:Collateral Sensitivity Associated with Antibiotic Resistance Plasmids
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Project description:Fluoroquinolone antibiotics, a common antibiotic for the treatment of Pseudomonas aeruginosa infection, are facing challenges due to the rapid evolution of bacterial resistance. Through designed evolutionary experiments in vitro, we find that there are significant differences in evolutionary trajectories and outcomes of resistant bacteria obtained in different induction modes, among which fitness benefit of resistant strains obtained in high-dose induction mode under high level of antibiotic is significantly higher than that of wild-type strain, and collateral sensitivity to aminoglycosides and some other antibiotics will be obtained. Resistance strains obtained in the low-dose induction mode exhibit higher heterogeneity, which is accompanied by multiple drug resistance (MDR). Through second generation resequencing and proteomic techniques, overexpression of MexCD-OprJ efflux pump induced by mutations in the nfxB gene significantly improved the fitness benefit of Pseudomonas aeruginosa PAO1 under high level of fluoroquinolones. This is the precondition of the further evolution of the fleroxacin-resistant strains in the high dose induction mode, the addition of the efflux pump inhibitor phenylalanyl arginyl β-naphthylamide (PAβN) could effectively repress the evolution of bacterial resistance in the high dose induction mode. Fleroxacin use followed by gentamicin helped drive infectious P.aeruginosa to extinction, causing nfxB mutation to cause collateral sensitivity to gentamicin.
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Project description:Exploiting Temporal Collateral Sensitivity in Tumor Clonal Evolution
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Project description:Collateral sensitivity of antibiotic resistant bacteria to antimicrobial peptides
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Project description:In this study, we combine MspJI digestion and electrophoretic band selection with next generation high-throughput sequencing technology to detect 5-methylcytosines in Arabidopsis genome. By developing a bioinformatics workflow to attribute the CNNR sites recognized by MspJI to the reference genome, we fulfilled the systematic assessment of this method. According to the assessment, here we provide the method for generating a detailed map of plant methylome that could be feasible, reliable and economical in methylation investigation. Extracting the MspJI digested fragments, constructing sequencing library according to the Illumina protocol and sequencing with Illumina HiSeq2000. Repeatability and reproducibility studies were performed between two samples from the same individual. Specificity and sensitivity of the method was examined by comparing our data with WGBS data downloaded from GEO (GSE15922: GSM399600). **The WGBS seq data ('aerial_tissues_BS_seq_CNNR.gff') was generated from the GSM399600 Sample supplementary files ('aerial_tissues_BS_seq_alignment_batch-*.gff.gz') and was utilized to do comparative study with our MspJI-seq data including sensitivity and specificity analysis.
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