Early rapid changes in response to the phytohormone abscisic acid (ABA) have been observed at the transcript level, but little is known how these transcript changes translate to changes in protein abundance under the same conditions. Here we have performed a global quantitative analysis of transcript and protein changes in Arabidopsis suspension cells in response to ABA using microarrays and quantitative proteomics. In summary, 3494 transcripts and 50 proteins were significantly regulated by ABA over a treatment period of 2024 h. Abscisic acid also caused a rapid and strong increase in production of extracellular reactive oxygen species (ROS) with an average half-rise time of 33 sec. A subset of ABA-regulated transcripts were differentially regulated in the presence of the ROS scavenger dimethylthiourea (DMTU) as compared with ABA alone, suggesting a role for ROS in the regulation of these ABA-induced genes. Transcript changes showed an overall poor correlation to protein changes (r = 0.66). Only a subset of genes was regulated at the transcript and protein level, including known ABA marker genes. We furthermore identified ABA regulation of proteins that function in a branch of glucosinolate catabolism previously not associated with ABA signaling. The discovery of genes that were differentially regulated at the transcript and at the protein level emphasizes the strength of our combined approach. In summary, our dataset not only expands previous studies on gene and protein regulation in response to ABA, but rather uncovers unique aspects of the ABA regulon and gives rise to additional mechanisms regulated by ABA.
Quantitative transcriptomic analysis of abscisic acid-induced and reactive oxygen species-dependent expression changes and proteomic profiling in Arabidopsis suspension cells.
Age, Specimen part, Cell line, Time
View SamplesThe Murphy Roth Large (MRL) mouse, a strain capable of regenerating right ventricular myocardium, has a high post-myocardial infarction (MI) survival rate compared with C57BL6/J (C57) mice. The biological processes responsible for this survival advantage are unknown.
Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic background.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A distinct microRNA signature for definitive endoderm derived from human embryonic stem cells.
Cell line, Time
View SamplesTotal RNA microarray data from Fresh-Frozen Glioblastoma tumor samples.
Epigenetic suppression of EGFR signaling in G-CIMP+ glioblastomas.
Specimen part, Disease stage
View SamplesHigh-fat diet (HFD) in normoxia causes a worsened phenotype in adult female flies compared to regular diet (RD). Intermittent hypoxia (IH) causes an opposite phenotype both when flies are on RD in IH compared to normoxia and even more dramatically when on HFD in IH compared to HFD in normoxia.
No associated publication
Sex, Specimen part
View SampleshESCs can differentiate into the three primary embryonic lineages (endoderm, mesoderm, ectoderm) as well as extraembryonic tissues. Definitive endoderm (DE) is the first step into the pathway to endoderm derived tissues: pancreas, liver, gut, lung.
A distinct microRNA signature for definitive endoderm derived from human embryonic stem cells.
Cell line, Time
View SamplesChanges occur in the lung epithelium after allergen challenge that may give insight into asthma pathogenesis and we sought to identify novelepithelial genes induced by allergen exposure.
Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.
Age, Specimen part
View SamplesPlant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed death acids. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.
Maize death acids, 9-lipoxygenase-derived cyclopente(a)nones, display activity as cytotoxic phytoalexins and transcriptional mediators.
Specimen part
View SamplesHigh-fat diet (HFD) in normoxia causes a worsened phenotype in adult female flies compared to regular diet (RD).
No associated publication
Sex, Specimen part
View SamplesTo evaluate gene expression profiles on different dendritic cell subsets isolated from spleens of mice
CD28 Deficiency Enhances Type I IFN Production by Murine Plasmacytoid Dendritic Cells.
Sex
View Samples