Heat stress is one of the most prominent and deleterious environmental threads affecting plant growth and development. Upon high temperatures, plants launch specialized gene expression programs that promote stress protection and survival. These programs involve global and specific changes at the transcriptional and translational levels. However the coordination of these processes and their specific role in the establishment of the heat stress response is not fully elucidated.
Analysis of genome-wide changes in the translatome of Arabidopsis seedlings subjected to heat stress.
Specimen part
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The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Alteration of Gene Expression, DNA Methylation, and Histone Methylation in Free Radical Scavenging Networks in Adult Mouse Hippocampus following Fetal Alcohol Exposure.
Sex, Specimen part, Treatment
View SamplesMouse models of Fetal Alcohol Spectrum Disorder can be used to assess molecular changes underlying the disorder. Neonatal ethanol exposure in mice can be used to model third trimester ethanol exposure in humans.
Alteration of Gene Expression, DNA Methylation, and Histone Methylation in Free Radical Scavenging Networks in Adult Mouse Hippocampus following Fetal Alcohol Exposure.
Sex, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
No sample metadata fields
View SamplesTwo rat hepatic cell lines, WB-F344 and WB311, were characterized for the effect of rapamycin on gene expression. The WB311 cell line, which is tumorigenic and resistant to the growth inhibitory effects of rapamycin, was originally derived from the WB-F344 parental hepatic epithelial cell line. The goal of this experiment was to identify genes that responded to rapamycin in the sensitive cells but not the resistant cells, thereby providing insight into the mechanism of rapamycin resistance.
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
No sample metadata fields
View Samples18 different population of cells in different developmental stages in hematopoietic hierarchy have been purifyed by FACS analyses from wild type C57Bl6 mice and subjected to Micrroarray Affymetrix mouse 430.2 platform
CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.
No sample metadata fields
View SamplesEarlier work has shown that pre-B cells can be converted into macrophages by the transcription factor C/EBP? at very high frequencies. Using this system we have now performed a systematic analysis of the question whether during transdifferentiation the cells transiently reactivate progenitor restricted genes or even retrodifferentiate. A transcriptome analysis of transdifferentiating cells showed that most genes are continuously up or downregulated, acquiring a macrophage phenotype within 5 days. In addition, we observed the transient reactivation of a subset of immature myeloid markers, as well as low levels of the progenitor markers Kit and Flt3 and a few lineage inappropriate genes. However, we were unable to observe the re-expression of cell surface marker combinations that characterize hematopoietic stem and progenitor cells (HSPCs), including c-Kit and Flt3. This was the case even when C/EBPalpha was activated in pre-B cells under culture conditions that favor HSPC growth or when the transcription factor was activated in a time limited fashion. Together, our findings are consistent with the notion that the conversion from pre-B cells to macrophages is mostly direct and does not involve overt retrodifferentiation.
CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.
Specimen part, Time
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