Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355973 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5069793.fastq.gz | Fastqsanger.gz | |||
| SRR5069794.fastq.gz | Fastqsanger.gz | |||
| SRR5069795.fastq.gz | Fastqsanger.gz | |||
| SRR5069796.fastq.gz | Fastqsanger.gz | |||
| SRR5069797.fastq.gz | Fastqsanger.gz |
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Project description:It is known that CBFB-MYH11, the fusion gene generated by inversion of chromosome 16 in human acute myeloid leukemia, is causative for oncogenic transformation. However, the mechanism by which CBFB-MYH11 initiates leukemogenesis is not clear. Previously published reports showed that CBFB-MYH11 dominantly inhibits RUNX1 and CBFB, and such inhibition has been suggested as the mechanism for leukemogenesis. However, knockin mice expressing Cbfb-MYH11 (Cbfb+/MYH11) showed defects in primitive hematopoiesis not seen in Cbfb null (Cbfb-/-) embryos indicating that Cbfb-MYH11 has repression independent activities as well. To identify gene expression changes associated with this novel activity, we compared the gene expression profile in the blood cells of Cbfb+/MYH11 and Cbfb-/- embryonic day 12.5 (E12.5) embryos with that of their wildtype littermates. Cbfb-MYH11 chimeras were mated to C57/Bl6 females to generate Cbfb+/MYH11 (Cbfb+/MYH11) and Cbfb+/+ (WT) embryos. Cbfb+/- x Cbfb+/- matings were used to generate Cbfb+/+ (Cbfb+/+) and Cbfb-/- (Cbfb-/-) embryos. Blood from 8-10 E12.5 embryos of the same genotype was pooled, and RNA was isolated, labeled, and hybridized to Affymetrix Genechip mouse microarray (430 2.0) chips. 4 chips were used for both the Cbfb+/MYH11 and littermate control samples. 3 chips were used for the Cbfb-/- samples and littermate control samples.
2010-04-12 | E-GEOD-19194 | biostudies-arrayexpress
Project description:Genome-wide maps of SATB1 bound regions in thymocytes and peripheral CD4+ T lymphocytes.
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Project description:It is known that CBFB-MYH11, the fusion gene generated by inversion of chromosome 16 in human acute myeloid leukemia, is causative for oncogenic transformation. However, the mechanism by which CBFB-MYH11 initiates leukemogenesis is not clear. Previously published reports showed that CBFB-MYH11 dominantly inhibits RUNX1 and CBFB, and such inhibition has been suggested as the mechanism for leukemogenesis. However, knockin mice expressing Cbfb-MYH11 (Cbfb+/MYH11) showed defects in primitive hematopoiesis not seen in Cbfb null (Cbfb-/-) embryos indicating that Cbfb-MYH11 has repression independent activities as well. To identify gene expression changes associated with this novel activity, we compared the gene expression profile in the blood cells of Cbfb+/MYH11 and Cbfb-/- embryonic day 12.5 (E12.5) embryos with that of their wildtype littermates.
2010-03-31 | GSE19194 | GEO
Project description:Ptf1a is a lineage-specific basic-helix-loop-helix transcription factor critical in the development of both the pancreas and nervous system. How one transcription factor controls diverse programs of gene expression is a fundamental question in developmental biology. To uncover molecular strategies for the program-specific functions of Ptf1a, we identified bound genomic regions in vivo during development of both tissues. A majority of regions bound by Ptf1a are tissue-specific, lie near genes needed for proper formation and maturation of each tissue, and reflect regions of open chromatin.M-BM- M-BM- Information for the specificity of Ptf1a binding and function is encoded in the DNA surrounding the Ptf1a-bound sites, since Ptf1a-bound regions are sufficient to direct tissue-restricted reporter expression when tested in transgenic mice. Fox and Sox factors were identified as lineage specific modifiers ofM-BM- Ptf1a binding, sinceM-BM- binding motifs for these factors are enriched in Ptf1a-bound regions in pancreas and neural tube, respectively. Although Ptf1a and Foxa2 co-localize to sites in embryonic pancreas and can act synergistically in cell transfection assays, biochemical experiments detected no physical interaction between the two factors. These findingsM-BM- indicateM-BM- that lineage-specific chromatin landscapes likely constrain the functions of Ptf1a, and identify Fox and Sox gene families as part of this process. RNA-Seq: Examination of gene expression in Ptf1a expressing cells (NT E.12.5, Pancreas E15.5) ChIP-Seq: Examination of chromatin occupancy in 2 tissue types (E12.5 NT and 17.5 Pancreas). Faire-Seq: Examination of open chromatin in 2 tissue types (E12.5 NT and 17.5 Pancreas).
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Project description:The C-terminus of CBFß-SMMHC, the fusion protein produced by a chromosome 16 inversion in acute myeloid leukemia subtype M4Eo, contains domains for self-mulimerization and transcriptional repression, both of which have been proposed to be important for leukemogenesis by CBFß-SMMHC. To test the role of the fusion protein's C-terminus in vivo, we generated knock-in mice expressing a C-terminally truncated CBFß-SMMHC (CBFß-SMMHCΔC95). Embryos with a single copy of CBFß-SMMHCDC95 were viable and showed no defects in hematopoiesis, while embryos homozygous for the CBFß-SMMHCΔC95 allele had hematopoietic defects and died in mid-gestation, similar to embryos with a single-copy of the full-length CBFß-SMMHCΔC95. To identify gene expression changes induced by CBFß-SMMHCDC95, we compared the gene expression profile in the blood cells of Cbfb+/+, Cbfb+/ΔC95, and CbfbΔC95/ΔC95 embryonic day 12.5 (E12.5) mice. Cbfb+/ΔC95 were mated together to generate Cbfb+/+, Cbfb+/ΔC95, and CbfbΔC95/ΔC95 embryos. Blood from 8-10 E12.5 embryos of the same genotype was pooled, and RNA was isolated, labeled, and hybridized to Affymetrix Genechip mouse microarray (430 2.0) chips. 3 chips were used for each genotype.
2013-02-19 | E-GEOD-42238 | biostudies-arrayexpress
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