Plant respiration responses to elevated growth [CO2] are key uncertainties in predicting future crop and ecosystem function. In particular, the effects of elevated growth [CO2] on respiration over leaf development are poorly understood. This study tested the prediction that, due to greater whole-plant photoassimilate availability and growth, elevated [CO2] induces transcriptional reprogramming and a stimulation of nighttime respiration in leaf primordia, expanding leaves, and mature leaves of Arabidopsis thaliana. In primordia, elevated [CO2] altered transcript abundance, but not for genes encoding respiratory proteins. In expanding leaves, elevated [CO2] induced greater glucose content and transcript abundance for some respiratory genes, but did not alter respiratory CO2 efflux. In mature leaves, elevated [CO2] led to greater glucose, sucrose and starch content, plus greater transcript abundance for many components of the respiratory pathway, and greater respiratory CO2 efflux. Therefore, growth at elevated [CO2] stimulated dark respiration only after leaves transitioned from carbon sinks into carbon sources. This coincided with greater photoassimilate production by mature leaves under elevated [CO2] and peak respiratory transcriptional responses. It remains to be determined if biochemical and transcriptional responses to elevated [CO2] in primordial and expanding leaves are essential prerequisites for subsequent alterations of respiratory metabolism in mature leaves.
Developmental stage specificity of transcriptional, biochemical and CO2 efflux responses of leaf dark respiration to growth of Arabidopsis thaliana at elevated [CO2].
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View SamplesTranscriptional reprogramming and stimulation of leaf respiration by elevated CO2 concentration is diminished, but not eliminated, under limiting nitrogen supply.
Transcriptional reprogramming and stimulation of leaf respiration by elevated CO2 concentration is diminished, but not eliminated, under limiting nitrogen supply.
Age, Specimen part
View SamplesProtein C (PC) deficiency increases the risk of venous thrombosis (VT) among members of Kindred Vermont II, but fails to fully account for the inheritance pattern. A genome scan of the pedigree supported the presence of a prothrombotic gene on chromosome 11q23 with weaker support on chromosomes 10p12 and 18p11.2-q11.
Cell adhesion molecule 1: a novel risk factor for venous thrombosis.
Sex, Age, Specimen part, Race
View SamplesCrossing of hDMD mice that contain the full-length 2.3 Mb hDMD gene were crossed with dystrophin-deficient mdx mice and dystrophin and utrophin double-deficient mdx x utrn-/- mice resulted in a full rescue of the dystrophic features of these mice, as concluded from histological analysis. Analysis on Affymetrix gene chips demonstrated that also expression profiles of the dystrophic mice were normalized by crossing with transgenic hDMD mice. This confirms the full functionality of the hDMD transgene in mice.
Generation and characterization of transgenic mice with the full-length human DMD gene.
No sample metadata fields
View SamplesThe aim of the present study was to compare, on a statistical basis, the performance of different microarray platforms to detect differences in gene expression in a realistic and challenging biological setting. Gene expression profiles in the hippocampus of five wild-type and five transgenic C-doublecortin-like kinase mice were evaluated with five microarray platforms: Applied Biosystems, Affymetrix, Agilent, Illumina and home-spotted oligonucleotide arrays. We observed considerable overlap between the different platforms, the overlap being better detectable with significance level-based ranking than with a p-value based cut-off. Confirming the qualitative agreement between platforms, Pathway analysis consistently demonstrated aberrances in GABA-ergic signalling in the transgenic mice, even though pathways were represented by only partially overlapping genes on the different platforms.
Can subtle changes in gene expression be consistently detected with different microarray platforms?
No sample metadata fields
View SamplesThe sensation of hunger after a period of fasting and the sensation of satiety after eating is crucial to behavioral regulation of food intake, but the biological mechanisms regulating these sensations are incompletely understood. We studied the behavioral and physiological adaptation to fasting in the vinegar fly (Drosophila melanogaster). Here we show that flies demonstrated increased behavioral attraction to food odor when food-deprived with no corresponding increase in sensitivity in the peripheral olfactory system. Flies increased their food intake transiently in the post-fasted state, but returned to a stable baseline feeding level within 24 hr after return to food. This modulation in feeding was accompanied by a significant increase in the size of the crop organ of the digestive system, suggesting that fasted flies responded both by increasing their food intake and storing reserve food in their crop. The post-fasting feeding response was observed in both male and female flies of diverse genetic backgrounds. Expression profiling of head, body, and chemosensory tissues by microarray analysis revealed several hundred genes that are regulated by feeding state, including 247 genes in the fly head. We performed RNA interference-mediated knockdown of, takeout, one of the genes strongly downregulated by fasting in multiple tissues. When takeout was knocked down in all neurons the post-fasting feeding response was abolished. These observations suggest that a coordinated transcriptional response to internal physiological state may regulate both ingestive behaviors and chemosensory perception of food
Post-fasting olfactory, transcriptional, and feeding responses in Drosophila.
Specimen part, Treatment, Time
View SamplesHumoral responses of mice specifically deleted for Moz (a histone acetyltransferase) or c-Myb (a transcription factor) in B cells were aberrant. RNA-sequencing analysis was performed to assess gene expression differences compared to wild-type controls in germinal center B cells or plasmablasts. Overall design: Moz f/f Aicda1-Cre, Aicda1-Cre, Myb f/f Cd23-Cre, Mybf/f (no cre) mice were immunized with NP-KLH precipitated in alum and germinal center B cells were sort-purified. Secondary plasmablasts were sort-purified from immunized mice boosted with NP-KLH in PBS (Myb experiment). Two independent experiments were conducted.
Regulation of germinal center responses and B-cell memory by the chromatin modifier MOZ.
Specimen part, Subject
View SamplesMouse ES cells were differentiated for 6 days. Undifferentiated cells (d0) were compared to cells harvested at 24 hour timepoints (d1-d6).
Transcriptional profiling of mouse and human ES cells identifies SLAIN1, a novel stem cell gene.
Age, Specimen part, Cell line, Time
View SamplesUndifferentiated cells of different passage numbers (p19 and p128) were compared to cells differentiated in hanging drops for 5 days (d5 embryoid bodies) or expanded on gelatin coated dishes for a further 9 days (d14 embryoid bodies).
Transcriptional profiling of mouse and human ES cells identifies SLAIN1, a novel stem cell gene.
Age, Specimen part, Cell line, Time
View SamplesHGPS is a rare premature ageing disease, caused by a mutation in the LMNA gene, which activates a cryptic splice site, resulting in the production of a mutant lamin A isoform, called progerin. Sporadic usage of the same cryptic splice site has been observed with normal physiological aging. As it is unknown how HGPS causes premature ageing defects, we set out to determine the gene signature of both young healthy individuals, old healthy individuals, as well as HGPS patients.
Repression of the Antioxidant NRF2 Pathway in Premature Aging.
Specimen part, Disease
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