The behavior of yeast cells during industrial processes such as the production of beer, wine and bioethanol has been extensively studied. By contrast, our knowledge about yeast physiology during solid state processes, such as bread dough, cheese or cocoa fermentation remains limited. We investigated changes in the transcriptome of three genetically distinct Saccharomyces cerevisiae strains during bread dough fermentation. Our results show that regardless of the genetic background, all three strains exhibit similar changes in expression patterns. At the onset of fermentation, expression of glucose-regulated genes changes dramatically, and the osmotic stress response is activated. The middle fermentation phase is characterized by the induction of genes involved in amino acid metabolism. Finally, at the latest time point, cells suffer from nutrient depletion and activate pathways associated with starvation and stress response. Further analysis shows that genes regulated by the High Osmolarity Glycerol (HOG) pathway, the major pathway involved in the response to osmotic stress and glycerol homeostasis, are among the most differentially expressed genes at the onset of fermentation. More importantly, deletion of HOG1 and other genes of this pathway significantly reduces fermentation capacity. Together, our results demonstrate that cells embedded in a solid matrix such as bread dough suffer severe osmotic stress, and that a proper induction of the HOG pathway is critical for an optimal fermentation.
Dynamics of the Saccharomyces cerevisiae transcriptome during bread dough fermentation.
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No sample metadata fields
View SamplesTime and dose related expression profiles of rat right heart tissue in microsphere bead model for Pulmonary embolism
Transcriptional profile of right ventricular tissue during acute pulmonary embolism in rats.
No sample metadata fields
View SamplesMenisci play a vital role in load transmission, shock absorption and joint stability. The current dogma is that the menisci simply protects the cartilage and play no role in osteoarthritis (OA) unless they are injured. However, there is increasing evidence suggesting that OA menisci may not merely be bystanders in the disease process of OA. This study sought: 1) to determine the prevalence of meniscal degeneration in OA patients, 2) to examine gene expression in OA meniscal cells compared to normal control meniscal cells, and 3) to test the hypothesis that OA meniscal cells are different from normal meniscal cells.
Analysis of meniscal degeneration and meniscal gene expression.
Specimen part
View SamplesTumors of advanced gastric cancer patients were biopsied and subjected to gene expression profiling using the Affymetrix Human Genome U133 Plus 2.0 Arrays. Patients were then segregated into G1, G2 or G3 groups based on their tumor genomic profiles. Patients in the G1 and G3 cohorts were assigned SOX (oxaliplatin plus S-1) chemotherapy whereas those in the G2 cohort were given SP (cisplatin plus S-1) regimen.
Real-Time Tumor Gene Expression Profiling to Direct Gastric Cancer Chemotherapy: Proof-of-Concept "3G" Trial.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesThese gene expression microarrays were performed as part of a project aiming to integrate quantitative proteomic, gene expression and epigenetic data from the childhood brain tumor medulloblastoma.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene reactivation by 5-aza-2'-deoxycytidine-induced demethylation requires SRCAP-mediated H2A.Z insertion to establish nucleosome depleted regions.
Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesRepair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.
Annexin A2 links poor myofiber repair with inflammation and adipogenic replacement of the injured muscle.
Age, Specimen part
View SamplesGenome wide gene expression profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The sample treated with non target siRNA and PBS serves as control sample.
No associated publication
Specimen part, Disease, Disease stage, Cell line
View SamplesCells were treated with MK591 and gene expression was analyzed with Illumina bead chip array.
No associated publication
Specimen part, Cell line
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