Background: Progressive neurological dysfunction is a key aspect of human aging. Because of underlying differences in the aging of mice and humans, useful mouse models have been difficult to obtain and study. We have used gene-expression analysis and polymorphism screening to study molecular senescence of the retina and hippocampus in two rare inbred mouse models of accelerated neurological senescence (SAMP8 and SAMP10) that closely mimic human neurological aging, and in a related normal strain (SAMR1) and an unrelated normal strain (C57BL/6J).
Mechanisms of aging in senescence-accelerated mice.
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View SamplesArabidopsis fc2-1 mutants fail to properly de-etiolate after a prolonged period in the dark. Our goal was to monitor whole genome expression during the first 2 hours of de-etiolation to determine the cuase of this growth arrest.
Ubiquitin facilitates a quality-control pathway that removes damaged chloroplasts.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Embryonic stem cell potency fluctuates with endogenous retrovirus activity.
Specimen part, Cell line, Treatment
View SamplesSupT1, PBMC, or IMR90 cells were infected with an HIV-based vector (see Schroder et al., Cell 110:521-9) and the RNA isolated 48 hours after infection.
Retroviral DNA integration: ASLV, HIV, and MLV show distinct target site preferences.
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View SamplesWe compared gene expression from 2C::tomato+/- ES cells from Kdm1a wt and mutant ES cultures
Embryonic stem cell potency fluctuates with endogenous retrovirus activity.
Cell line
View SamplesA complex interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 is essential for triggering ethylene responses in plants.
Interplay between ethylene, ETP1/ETP2 F-box proteins, and degradation of EIN2 triggers ethylene responses in Arabidopsis.
Age, Treatment
View SamplesWe studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions
Adipocyte CREB promotes insulin resistance in obesity.
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View SamplesThe composition of chromatin remodeling complexes dictates how these enzymes control transcriptional programs and cellular identity. Here, we investigate the composition of SWI/SNF complexes in embryonic stem cells (ESCs). In contrast to differentiated cells, ESCs have a biased incorporation of certain paralogous SWI/SNF subunits, with low levels of Brm, BAF170 and ARID1B. Upon differentiation, the expression of these subunits increases, resulting in a higher diversity of compositionally distinct SWI/SNF enzymes. We also identify Brd7 as a novel component of the PBAF complex in both ESCs and differentiated cells. Using shRNA-mediated depletion of Brg1, we show that SWI/SNF can function as both a repressor and an activator in pluripotent cells, regulating expression of developmental modifiers and signaling components such as Nodal, ADAMTS1, Bmi-1, CRABP1 and TRH. Knock-down studies of PBAF-specific Brd7 and of a signature subunit within the BAF complex, ARID1A, show that these two sub-complexes affect SWI/SNF target genes differentially, in some cases even antagonistically. This may be due to their different biochemical properties. Finally, we examine the role of SWI/SNF in regulating its target genes during differentiation. We find that SWI/SNF affects recruitment of components of the pre-initiation complex in a promoter-specific manner, to modulate transcription positively or negatively. Taken together, our results provide insight into the function of compositionally diverse SWI/SNF enzymes that underlie their inherent gene-specific mode of action.
BRD7, a novel PBAF-specific SWI/SNF subunit, is required for target gene activation and repression in embryonic stem cells.
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View SamplesHuman 293T cells engineered to express the TVA receptor (see Mitchell et al., PLoS) infected with an ASLV vector. RNA isolated 48 hours later.
No associated publication
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View SamplesThe CREB family of transcription factors stimulates cellular gene expression following phosphorylation at a conserved serine (Ser133 in CREB1) in response to cAMP and other extracellular signals. In order to characterize CREB target genes in various tissues, we give a cAMP agonist, forskolin (FSK), to cell lines or primary cultures and monitor the gene expression. To eliminate CREB-independent effects of FSK on cellular gene expression, we employed a dominant negative form of CREB called A-CREB, which dimerizes selectively with and blocks the DNA binding activity of CREB but not other bZIP family members. Therefore, genes that are induced by cAMP and the induction was blocked by A-CREB treatment likely represents CREB target genes.
Genome-wide analysis of cAMP-response element binding protein occupancy, phosphorylation, and target gene activation in human tissues.
No sample metadata fields
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