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Expression data of leukemia samples taken from transgenic ERG mice

ABSTRACT: The Ets transcription factor, ERG, plays a central role in definitive hematopoiesis and its overexpression in acute myeloid leukemia is associated with a stem cell signature and bad prognosis. However, little is known about the underlying mechanism by which ERG causes leukemia. Therefore we sought to identify ERG targets that participate in development of leukemia by integration of expression arrays and Chromatin immunoprecipitation. Bone marrow was collected from three transgenic ERG mice harboring a myeloid leukemia and twelve wild type mice. Nine wild type bone marrow samples were lineage depleted and pooled into 3 samples (each one consisting of three lineage negative wild type bone marrows). The resulting 9 samples were used for RNA extraction and hybridization on affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: jasmine jacob

PROVIDER: E-GEOD-49787 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from transgenic ERG, GATA1s KI and ERG/GATA1s fetal livers

Project description:DS children have a 500-fold increased risk for developing acute megakaryoblastic leukemia (AMKL). Around 10% of DS newborns have a transient myeloproliferative disorder (TMD) that resolves spontaneously. Somatic mutations acquired during fetal hematopoiesis in the GATA1 transcription factor are detected in megakaryoblasts from all the DS TMDs or AMKLs. GATA1 is an X chromosome transcription factor essential for the development of multiple hematopoietic lineages. Loss of GATA1 results in embryonic lethality due to severe anemia. The GATA1 mutations result in the expression of a shorter isoform, GATA1s. Replacement of GATA1 with GATA1s causes transient proliferation of immature fetal megakaryocytic progenitors. The Hsa21 ETS transcription factor, ERG, is expressed in megakaryocytes and erythrocytes and is involved in several types of cancer. Mutation in GATA1 gene leading to expression of the short isoform (GATA1s) that occurs on the background of trisomy 21 is regarded as one of the driving forces for megakaryocytic expansion observed in DS fetal livers. ERG, which is located on chromosome 21, is considered one of the leading candidates to cooperate with GATA1 mutation in the generation of DS AMKL. To study the in vivo cooperation between ERG and GATA1 isoforms, we crossed the ERG transgenic mice with the GATA1s Knock-in mice (GATA null background). We found that males expressing both ERG and the short isoform of GATA1(GATA1s) died in uterus between embryonic days E121/2 and E141/2.We studied erythropoiesis and megakaryopoiesis in fetal livers from the different genotypes generated from our cross. We used expression array to study the specific interaction of ERG with the different GATA1 isoforms in fetal livers from E121/2 and E141/2 and identify ERG, GATA1 and GATA1s target genes by comparing sets of genes that are activated or repressed in the presence of ERG and the two isoforms of GATA1.

2013-12-31 | E-GEOD-46481 | biostudies-arrayexpress

Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR) [expression]

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2013-07-23 | E-GEOD-49100 | biostudies-arrayexpress

Identification of human nephron progenitors capable of generation of kidney structures and functional repair of chronic renal disease

Project description:NCAM1+ subpopulation of fetal human kidneyl cells are nephron progenitors We used microarrays to detail the global programme of gene expression in the NCAM1+ sub-population in comparison to total culture.

2013-07-23 | E-GEOD-49101 | biostudies-arrayexpress

Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR)

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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2011-12-31 | E-GEOD-28052 | biostudies-arrayexpress

Comparison of B6/D2 Whole Brain Alternative Splicing

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2011-09-19 | E-GEOD-22946 | biostudies-arrayexpress

Alu sequences in undifferentiated human embryonic stem cells display high levels of A-to-I RNA editing

Project description:Adenosine to Inosine (A-to-I) RNA editing is a site-specific modification of RNA transcripts, catalyzed by members of the ADAR (Adenosine Deaminase Acting on RNA) protein family. RNA editing occurs in human RNA in thousands of different sites. Some of the sites are located in protein-coding regions but the majority is found in non-coding regions, such as 3âUTRs, 5âUTRs and introns - mainly in Alu elements. While editing is found in all tissues, the highest levels of editing are found in the brain. It was shown that editing levels within protein-coding regions are increased during embryogenesis and after birth and that RNA editing is crucial for organism viability as well as for normal development. In this study we characterized the A-to-I RNA editing phenomenon during neuronal and spontaneous differentiation of human embryonic stem cells (hESCs). We identified high editing levels of Alu repetitive elements in hESCs and demonstrated a global decrease in editing levels of non-coding Alu sites when hESCs are differentiating, particularly into the neural lineage. Using RNA interference, we showed that the elevated editing levels of Alu elements in undifferentiated hESCs are highly dependent on ADAR1. DNA microarray analysis showed that ADAR1 knockdown has a global effect on gene expression in hESCs and leads to a significant increase in RNA expression levels of genes involved in differentiation and development processes, including neurogenesis. Taken together, our data suggest that A-to-I editing of Alu sequences plays a role in the regulation of hESC early differentiation decisions. Two samples, One control and the second treated

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