Ontology highlight
ABSTRACT:
PROVIDER: PRJNA932445 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23364800_1.fastq.gz | Fastqsanger.gz | |||
| SRR23364800_2.fastq.gz | Fastqsanger.gz | |||
| SRR23364801_1.fastq.gz | Fastqsanger.gz | |||
| SRR23364801_2.fastq.gz | Fastqsanger.gz | |||
| SRR23364802_1.fastq.gz | Fastqsanger.gz |
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Project description:To explore the possible changes of gene expression induced by a carcinogen, we treated wild-type and Dicer1-KO mice with one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU), a model genotoxic carcinogen, and vehicle control. The gene expression profiles were assessed in the mouse livers in wild-type and Dicer1-KO mice design. Total RNA were isolated from the livers at days 15 after the treatment and their expression was determined using Gene Array. Gene expression in treated wild-type and Dicer1-KO mice was measured at 15 days after exposure to one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU). Each treatment duplex ,Drug-ko-a,Drug-ko-b,Drug-wt-a,Drug-wt-b,Control-ko-a,Control-ko-b,Control-wt-a,Control-wt-b.
2012-03-06 | E-GEOD-36307 | biostudies-arrayexpress
Project description:To explore the possible changes of gene expression induced by a carcinogen, we treated wild-type and Dicer1-KO mice with one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU), a model genotoxic carcinogen, and vehicle control. The gene expression profiles were assessed in the mouse livers in wild-type and Dicer1-KO mice design. Total RNA were isolated from the livers at days 15 after the treatment and their expression was determined using Gene Array.
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Project description:We have generated mice that carry Cre-dependent "knock-in" alleles (MGS34F and IES34F) of U2af1(S34F), a mutation commonly encountered in human myelodysplastic syndromes and acute myeloid leukemia (AML). MEFs were generated from the progenies of these mice with those carrying a UBC-CreERT2 transgene, and were treated with 4-Hydroxytamoxifen (4OHT) to induce Cre-mediated recombination and subsequent U2af1(S34F) expression. Mice carrying the MGS34F allele were further crossed with those carrying a floxed Runx1 allele and Mx1-Cre. U2af1(S34F) expression and Runx1 deletion caused changes in gene expression and RNA splicing. Mice with a conditional "knock-in" U2af1(S34F) allele and conditional "knockout" alleles of Runx1 were mutagenized with low-dose N-Ethyl-N-Nitrosourea (ENU). Within 1.5 year, one of fourteen ENU-treated mice with U2af1(S34F) and Runx1 deletion developed AML, as did recipients of allografted splenic cells from two other such mice, but AML did not arise from cells with other genotypes or mice without ENU treatment.
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Project description:In this study, we exposed Caenorhabditis elegans wild types N2 to two concentrations of the model genotoxicants formaldehyde (HCHO), N-ethyl-N-nitrosourea (ENU), and methyl methanesulfonate (MMS).We performed a concentration-response test to determine the non-toxic concentration range for studying the transcriptional effects of compounds. In microarray experiments, we studied two concentrations (1 mM and 5 mM) for each compound and a control of M9 medium. Age synchronized worms at developmental L4 larval stage were exposed to treatment for four hours. After flash freezing the samples, RNA was isolated, labeled and hybridized on oligo microarray (Agilent) slides.
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Project description:Despite considerable progress understanding genes that affect the HDL particle, its function, and cholesterol content, genes identified to date explain only a small percentage of the genetic variation. We used N-ethyl-N-nitrosourea mutagenesis in mice to discover novel genes that affect HDL cholesterol levels. Two mutant lines (Hlb218 and Hlb320) with low HDL cholesterol levels were established. Causal mutations in these lines were mapped using linkage analysis: For line Hlb218 within a 12 Mbp region on Chr 10; and for line Hlb320 within a 17 Mbp region on Chr 7. High-throughput sequencing of Hlb218 liver RNA identified a mutation in Pla2g12b. The transition of G to A leads to a cysteine to tyrosine change and most likely causes a loss of a disulfide bridge. Microarray analysis of Hlb320 liver RNA showed a 7-fold downregulation of Hpn; sequencing identified a mutation in the 3M-bM-^@M-2 splice site of exon 8. Northern blot confirmed lower mRNA expression level in Hlb320 and did not show a difference in splicing, suggesting that the mutation only affects the splicing rate. In addition to affecting HDL cholesterol, the mutated genes also lead to reduction in serum non-HDL cholesterol and triglyceride levels. Despite low HDL cholesterol levels, the mice from both mutant lines show similar atherosclerotic lesion sizes compared to control mice. These new mutant mouse models are valuable tools to further study the role of these genes, their affect on HDL cholesterol levels, and metabolism. Mutant mice were generated as part of The Jackson LaboratoryM-bM-^@M-^Ys Heart, Lung, Blood, and Sleep Disorder Mutagenesis Program by treating male C57BL/6J (B6) mice with N-ethyl-N-nitrosourea (ENU). Third generation (G3) mice were phenotyped to ensure capture of both dominant and recessive mutations. Two unique G3 animals with low HDL cholesterol levels were then used to establish new inbred lines (Hlb218 and Hlb320) by mating them with B6 mice and intercrossing the offspring with low HDL cholesterol for 7 generations. Livers from 3 Hlb218, 3 Hlb320 males, and 6 B6 male controls were obtained for gene expression analysis. The samples were randomized over Illumina Mouse-6 Expression 1.1 BeadChips .
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Project description:Dysregulated expression of microRNA (miRNA) has been extensively detected in human cancer tissues and has shown promise in defining tumor status. It, however, is little known whether and when expression of miRNAs can be changed in normal tissues after carcinogen exposure. To explore possible time-course changes of miRNA expression induced by carcinogens, we treated mice with one dose of 120 mg/kg body weight model genotoxic carcinogen N-ethyl-N-nitrosourea (ENU) and vehicle control. The miRNA expression profiles were determined in the mouse livers in a time-course manner. MiRNAs were isolated from the livers of ENU-treated and control mice at days 1, 3, 7, 15, 30 and 120 after the treatment. The miRNA expressions were determined using RT2-mouse miRNA PCR Array. Principal component analysis of the gene expression profiles showed that miRNA expression at post-treatment days 7 and 15 were different from those at the other time points and the controls. The numbers of the dysregulated miRNAs changed with time, being 3, 5, 14, 32, 5 and 5 at post-treatment days 1, 3, 7, 15, 30 and 120, respectively. Functional analysis of the differentially expressed miRNA at post-treatment days 7 and 15 indicated that the major functions of these ENU-induced dysregulated miRNAs were mainly associated with DNA repair and tumorigenesis, suggesting the microRNA expression is related to genotoxicity of ENU. These results propose that one to two weeks after ENU exposure is the best time for miRNA expression sampling; and that a large number of miRNAs whose expression is dysregulated after carcinogen exposure could be an indicator for carcinogenic damage. Series type: Non-coding RNA profiling by RT-PCR
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