TRIAD
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB28011 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2720680_1.fastq.gz | Fastqsanger.gz | |||
| ERR2720680_2.fastq.gz | Fastqsanger.gz | |||
| ERR2720681_1.fastq.gz | Fastqsanger.gz | |||
| ERR2720681_2.fastq.gz | Fastqsanger.gz | |||
| ERR2720682_1.fastq.gz | Fastqsanger.gz |
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Project description:This study examined how transcriptomics tools can be included in a Triad-based soil quality assessment to assess the toxicity of soils from river banks polluted by metals. To that end we measured chemical soil properties and used the standardized ISO guideline for ecotoxicological tests and a newly developed microarray for gene expression in the indicator soil arthropod, Folsomia candida. Microarray analysis revealed that the oxidative stress response pathway was significantly affected in all soils except one. The data indicate that changes in cell redox homeostasis are a significant signature of metal stress. Finally, 32 genes showed significant dose-dependent expression with metal concentrations. They are promising genetic markers providing an early indication of the need for higher tier testing in soil quality. One of the least polluted soils showed toxicity in the bioassay that could be removed by sterilization. The gene expression profile for this soil did not show a metal-related signature, confirming that another factor than metals (most likely of biological origin) caused the toxicity. This study demonstrates the feasibility and advantages of integrating transcriptomics into Triad-based soil quality assessment. Combining molecular and organismal life-history traitM-bM-^@M-^Ys stress responses helps identifying causes of adverse effect in bioassays. Further validation is needed for verifying the set of genes with dose-dependent expression patterns linked with toxic stress. We used a one-color microarray design where each sample was hybridized to a single array
2014-02-01 | E-GEOD-52393 | biostudies-arrayexpress
Project description:This study examined how transcriptomics tools can be included in a Triad-based soil quality assessment to assess the toxicity of soils from river banks polluted by metals. To that end we measured chemical soil properties and used the standardized ISO guideline for ecotoxicological tests and a newly developed microarray for gene expression in the indicator soil arthropod, Folsomia candida. Microarray analysis revealed that the oxidative stress response pathway was significantly affected in all soils except one. The data indicate that changes in cell redox homeostasis are a significant signature of metal stress. Finally, 32 genes showed significant dose-dependent expression with metal concentrations. They are promising genetic markers providing an early indication of the need for higher tier testing in soil quality. One of the least polluted soils showed toxicity in the bioassay that could be removed by sterilization. The gene expression profile for this soil did not show a metal-related signature, confirming that another factor than metals (most likely of biological origin) caused the toxicity. This study demonstrates the feasibility and advantages of integrating transcriptomics into Triad-based soil quality assessment. Combining molecular and organismal life-history trait’s stress responses helps identifying causes of adverse effect in bioassays. Further validation is needed for verifying the set of genes with dose-dependent expression patterns linked with toxic stress.
2014-02-01 | GSE52393 | GEO
Project description:In our early study (PMID: 21939527), we have created a ClinicoMolecular Triad Classification (CMTC) to improve prediction and prognostication of breast cancer by using a training cohort contained 161 breast cancer patients (2003 to 2008). Here, a supplemental internal validation cohort contained 340 breast cancer patients was collected (2008 to 2010) for development of the CMTC.
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Project description:Somatic transposon mutagenesis in mice is an efficient strategy to investigate the genetic mechanisms of tumorigenesis. The identification of tumor driving transposon insertions traditionally requires the generation of large tumor cohorts to obtain information about common insertion sites. Tumor driving insertions are also characterized by their clonal expansion in tumor tissue, a phenomenon that is facilitated by the slow and evolving transformation process of transposon mutagenesis. We describe here an improved approach for the detection of tumor driving insertions that assesses the clonal expansion of insertions by quantifying the relative proportion of sequence reads obtained in individual tumors. To this end, we have developed a protocol for insertion site sequencing that utilizes acoustic shearing of tumor DNA and Illumina sequencing. We analyzed various solid tumors generated by PiggyBac mutagenesis and for each tumor >10^6 reads corresponding to >10^4 insertion sites were obtained. In each tumor, 9 to 25 insertions stood out by their enriched sequence read frequencies when compared to frequencies obtained from tail DNA controls. These enriched insertions are potential clonally expanded tumor driving insertions, and thus identify candidate cancer genes. The candidate cancer genes of our study comprised many established cancer genes, but also novel candidate genes such as Mastermind-like1 (Mamld1) and Diacylglycerolkinase delta (Dgkd). We show that clonal expansion analysis by high-throughput sequencing is a robust approach for the identification of candidate cancer genes in insertional mutagenesis screens on the level of individual tumors. Solid tumors in mice were generated by somatic transposon mutagenesis with a PiggyBac transposon system. Insertion sites of transposons in 11 tumors and 6 non-cancerous tail controls were determined by Illumina high-throughput sequencing. Insertions were determined both on 5' and 3' sides of the transposon (PB5 and PB3, respectively). Quantitative analysis of read numbers revealed enrichment of certain insertions in tumors, but not in controls, and these enriched insertions identify candidate cancer genes.
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Project description:Deep indel mutagenesis reveals the impact of insertions and deletions on protein stability and function
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Project description:In this work, a plasmid-based system is applied to inhibit the transposition of bacterial insertion sequences (IS). Using multiple guide RNAs, inactivated Cas9 was directed to simultaneously bind to the left end of IS1, IS5, IS3 and IS150 in Escherichia coli, in vivo. As a result, the transcription of IS1, and IS5 was successfully silenced, in certain cases by two orders of magnitude. The transposition rate of all four targeted elements nevertheless dropped to negligible levels, as verified at the cycA and bgl chromosomal loci. A GFP-expressing plasmid, known to be predominantly inactivated by insertion mutations also displayed a significant increase in stability. The transposition-silencing effect was easily transferable between various E. coli strains by plasmid transformation. Our portable system, or other plasmids constructed likewise can serve as useful tools to eliminate insertion mutagenesis or selectively study distinct transposable elements in numerous prokaryotic species.
2019-02-21 | GSE110946 | GEO
Project description:This dataset was used to assess the random insertion by tranposases of lox sites in Mycoplasma pneumoniae. This is part of the protocol LoxTnSeq, a new methodology to generate and catalogue libraries of genome reduction mutants. LoxTnSeq combines random integration of Lox sites by transposon mutagenesis, and the generation of mutants via cre recombinase, catalogued via deep-sequencing. When LoxTnSeq was applied to the naturally genome reduced bacterium Mycoplasma pneumoniae, we obtained a mutant pool containing 285 unique deletions. These deletions spanned from >50 bp to 28 Kb, which represent 21% of the total genome. LoxTnSeq also highlighted large regions of non-essential genes that could be removed simultaneously, and other similar regions that could not, providing a guide for future genome reductions.
2021-08-18 | E-MTAB-9590 | biostudies-arrayexpress
Project description:We present LoxTnSeq, a new methodology to generate and catalogue libraries of genome reduction mutants. LoxTnSeq combines random integration of Lox sites by transposon mutagenesis, and the generation of mutants via cre recombinase, catalogued via deep-sequencing. When LoxTnSeq was applied to the naturally genome reduced bacterium Mycoplasma pneumoniae, we obtained a mutant pool containing 285 unique deletions. These deletions spanned from >50 bp to 28 Kb, which represent 21% of the total genome. LoxTnSeq also highlighted large regions of non-essential genes that could be removed simultaneously, and other similar regions that could not, providing a guide for future genome reductions.
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Project description:Somatic transposon mutagenesis in mice is an efficient strategy to investigate the genetic mechanisms of tumorigenesis. The identification of tumor driving transposon insertions traditionally requires the generation of large tumor cohorts to obtain information about common insertion sites. Tumor driving insertions are also characterized by their clonal expansion in tumor tissue, a phenomenon that is facilitated by the slow and evolving transformation process of transposon mutagenesis. We describe here an improved approach for the detection of tumor driving insertions that assesses the clonal expansion of insertions by quantifying the relative proportion of sequence reads obtained in individual tumors. To this end, we have developed a protocol for insertion site sequencing that utilizes acoustic shearing of tumor DNA and Illumina sequencing. We analyzed various solid tumors generated by PiggyBac mutagenesis and for each tumor >10^6 reads corresponding to >10^4 insertion sites were obtained. In each tumor, 9 to 25 insertions stood out by their enriched sequence read frequencies when compared to frequencies obtained from tail DNA controls. These enriched insertions are potential clonally expanded tumor driving insertions, and thus identify candidate cancer genes. The candidate cancer genes of our study comprised many established cancer genes, but also novel candidate genes such as Mastermind-like1 (Mamld1) and Diacylglycerolkinase delta (Dgkd). We show that clonal expansion analysis by high-throughput sequencing is a robust approach for the identification of candidate cancer genes in insertional mutagenesis screens on the level of individual tumors.
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