Oocyte maturation is accompanied by a transition from mRNA stability to instability. We investigated the role of DCP1A and DCP2, proteins responsible for mRNA decapping, in mRNA destabilization during mouse oocyte maturation.
Maternally recruited DCP1A and DCP2 contribute to messenger RNA degradation during oocyte maturation and genome activation in mouse.
No sample metadata fields
View SamplesAims: We investigate sex differences and the role of oestrogen receptor beta (ERbeta) in a mouse model of pressure overload-induced myocardial hypertrophy. Methods and results: We performed transverse aortic constriction (TAC) or sham surgery in male and female wild-type (WT) and ERbeta knockout (ERbeta-/-) C57Bl6 mice. All mice were characterised by echocardiography and haemodynamic measurements and were sacrificed nine weeks after surgery. Left ventricular (LV) samples were analysed by microarray profiling, real-time RT-PCR and histology. After nine weeks, WT males showed more hypertrophy and heart failure signs than WT females. Notably, WT females developed a concentric form of hypertrophy, while males developed eccentric hypertrophy. These sex differences were abolished in ERbeta-/- mice. ERbeta deletion augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene expression profiling revealed that male WT hearts had a stronger induction of matrix-related genes and a stronger repression of mitochondrial genes than female hearts. ERbeta-/- mice exhibited a different transcriptome. Induction of pro-apoptotic genes after TAC occurred in ERbeta-/- mice of both sexes with a stronger expression in ERbeta-/- males. Histological analysis revealed, that cardiac fibrosis was more pronounced in male WT TAC than in female mice. This was abolished in ERbeta-/- mice. Apoptosis was significantly induced in both sexes of ERbeta-/- TAC mice, but it was most prominent in males. Conclusion: Female sex offers protection against ventricular chamber dilation in the TAC model. Both the female sex and ERbeta attenuate the development of fibrosis and apoptosis; thus slowing the progression to heart failure.
Female sex and estrogen receptor-beta attenuate cardiac remodeling and apoptosis in pressure overload.
Sex, Age, Specimen part
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesPU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation.
Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
X chromosome control of meiotic chromosome synapsis in mouse inter-subspecific hybrids.
Specimen part
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