Project description:Soluble pyridine nucleotide transhydrogenase (EcSthA) derived from Escherichia coli was introduced into the L-malic acid producing strain MA009-5 of Pichia kudriavzevii to obtain strain MA009-10. It was found that MA009-10 was superior to MA009-5 in terms of L-malic acid titer, glucose consumption rate, and glucose/L-malic acid conversion rate. To elucidate the effect of EcSthA expression on L-malic acid synthesis, we analyzed the RNA-seq data of both strains.
Project description:Primary objectives: Characterization of the macrophage population subset that is modulated by enteric neurons
Primary endpoints: Characterization of the macrophage population subset that is modulated by enteric neurons via RNA sequencing
| 2538227 | ecrin-mdr-crc
Project description:Microbial community of grape rhizosphere with malic acid
Project description:Differential gene expression analysis of five different strains of Crabtree-negative Saccharomyces cerevisiae that lack pyruvate decarboxylase activity. The three different acids studied were lactic, malic, and 3-hydroxypropionic acid.
Project description:L. oligofermentans was grown microaerobically on modified (without malic acid, cellulose and bromocresol green) MLD medium (Cavin JF et al., Appl Environ Microbiol 1989), containing either glucose, ribose or xylose as a sole carbon source (50mM) in three replicates. Samples were taken at three time points 20 h, 24 h and 30 h. RNA extraction and RNA sequencing libraries construction were done as described in Andreevskaya M et al., Appl Environ Microbiol 2015. Libraries were sequenced in two runs with six lanes overall using SOLiD 5500XL to produce 75 bp single-end reads. Obtained .xsq files were converted into .fastq files.
Project description:Malic enzymes decarboxylate the tricarboxylic acid (TCA) cycle intermediate malate to the glycolytic end-product pyruvate and are well positioned to regulate metabolic flux in central carbon metabolism. The bacterium Sinorhizobium meliloti has a NAD(P)-malic enzyme (DME) and a NADP-malic enzyme (TME) and DME is required for symbiotic N2-fixation. To help understand the role of these enzymes, we examined growth, metabolic and transcriptional consequences resulting from the deletion of these enzymes. Few effects were observed upon growth with glucose, whereas growth with the gluconeogenic substrate, succinate, resulted in transcriptional and metabolic effects particularly in the dme mutant strains. When grown with succinate, DME mutant cells accumulated hexose sugar phosphates and trehalose, while TME mutants accumulated putrescine. Succinate-grown DME mutant cells also showed increased transcription of genes for gluconeogenesis and for pathways such as amino acid and fatty acid synthesis that divert metabolites away from the TCA cycle. These data suggested that, DME is required to regulate the levels of TCA cycle intermediates and that the activity of TME is insufficient to prevent the accumulation of TCA cycle intermediates in cells utilizing succinate as carbon source. Consistent with this, in short-1-3 hour incubations with succinate, dme mutant cells excreted large amounts of malate whereas little malate was excreted from tme or wild-type cells. These results support the suggestion that DME is required for N2-fixation in alfalfa because it is required for synthesis of pyruvate and acetyl-CoA and the rapid metabolism of C4-dicarboxylates supplied by the plant. RNA expression was measured for S. meliloti in exponential phase grown in MOPS (morpholinpropanesulfonic acid) buffered minimal media under 2 growth conditions: 1) 15 mM succinate, 2) 15 mM glucose; using wild type cells as well as dme and tme mutant strains (6 experiments, 2 replicates: total 12 samples)
Project description:Goal of this study was to investigate the metabolic adaptation of C. auris to different carbon sources (malic acid, α-ketoglutarate, proline) and nitrogen sources (dipeptides). As a control medium with glucose as carbon source and ammonium sulfate as nitrogen source was used. Transcriptional profiles were compared after 4 h incubation at 37°C.
Project description:Goal of this study was to investigate the metabolic adaptation of C. albicans to different carbon sources (malic acid, α-ketoglutarate, proline) and nitrogen sources (dipeptides). As a control medium with glucose as carbon source and ammonium sulfate as nitrogen source was used. Transcriptional profiles were compared after 4 h incubation at 37°C.
Project description:Macrophage-mediated inflammation is a major contributor to obesity-associated insulin resistance. The corepressor NCoR interacts with inflammatory pathway genes in macrophages, suggesting that its removal would result in increased activity of inflammatory responses. Surprisingly, we find that macrophage-specific deletion of NCoR instead results in an anti-inflammatory phenotype along with robust systemic insulin sensitization in obese mice. We present evidence that de-repression of LXRs contributes to this paradoxical anti-inflammatory phenotype by causing increased expression of genes that direct biosynthesis of palmitoleic acid and M-OM-^I3 fatty acids. Remarkably, the increased M-OM-^I3 fatty acid levels primarily inhibit NF-M-NM-:B-dependent inflammatory responses by uncoupling NF-M-NM-:B binding and enhancer/promoter histone acetylation from subsequent steps required for pro-inflammatory gene activation. This provides a mechanism for the in vivo anti-inflammatory insulin sensitive phenotype observed in mice with macrophage-specific deletion of NCoR. Therapeutic methods to harness this mechanism could lead to a new approach to insulin sensitizing therapies. ChIP-Seq and Gro-Seq profiling was performed in thioglycollate-elicited peritoneal macrophages treated as indicated.