Project description:Transcript profiling of control vs Mungbean yellow mosaic India virus infected Glycine max variety JS335. RNA samples were collected at 2 dpi to study change in transcript profile at early infection.
Project description:Transcript profiling of control vs Mungbean yellow mosaic India virus infected Glycine max variety JS335. RNA samples were collected at 2 dpi to study change in transcript profile at early infection. Two-condition experiment, control vs. MYMIV infected.
Project description:Purpose: The goals of this study are to analyze primary myoblast cell from mdx mice skeletal muscle transcriptome profiling (RNA-seq) treated with different concentration glycine. Methods: primary myoblast cell isolated from 6-8-week-old mdx mice limb skeletal muscle and the primary myoblast treated with 0.2mM or 0.8mM glycine 24-hour. Primary myoblast mRNA profiles of 0.2mM glycine treated(3 replicates) and 0.8mM glycine treated(6 replicates) were generated by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed at the gene level using HISAT2 and StringTie followed by DESeq2.
Project description:These data belong to a metabolic engineering project that introduces the reductive glycine pathway for formate assimilation in Cupriavidus necator. As part of this project we performed short-term evolution of the bacterium Cupriavidus necator H16 to grow on glycine as sole carbon and energy source. Some mutations in a putiative glycine transporting systems facilitated growth, and we performed transcriptomics on the evolved strain growing on glycine. Analysis of these transcriptomic data lead us to the discovery of a glycine oxidase (DadA6), which we experimentally demonstrated to play a key role in the glycine assimilation pathay in C. necator.
Project description:Genome wide DNA methylation profiling of Jurkat T lymphoma cell lines, using the human DNA methylationEPIC 850K array. All cells were blocked using a thymidine block, and DNA methylation was analysed 4 hrs post release from the block (S-Phase) or 72 hours later. Samples are either untreated control (PBS) or treated with Glycine chloramine. Cells were exposed to Glycine chloramine in two independent time points: pre replication (same time as release from block, 3 replicates) or during S-phase (four replicates, 2 hrs post block release). These two exposures were assessed in two independent experiments and therefore have their own controls. Each replicate used cells from a different passage number, and was performed independently.
Project description:We use RNA sequencing technology in a time course study to measure transcript abundance from three developmental stages in cotyledons and five stages in the trifoliate leaf of Glycine max to identify genes with distinct temporal patterns of expression during leaf or cotyledon development. We also examine the diffrences between these two photosynthetic tissues.
Project description:Soybean (Glycine max) seeds are an important source of seed storage compounds, including protein, oil, and sugar used for food, feed, chemical, and biofuel production. We assessed detailed temporal transcriptional and metabolic changes in developing soybean embryos to gain a systems biology view of developmental and metabolic changes and to identify potential targets for metabolic engineering. Two major developmental and metabolic transitions were captured enabling identification of potential metabolic engineering targets specific to seed filling and to desiccation. The first transition involved a switch between different types of metabolism in dividing and elongating cells. The second transition involved the onset of maturation and desiccation tolerance during seed filling and a switch from photoheterotrophic to heterotrophic metabolism. Clustering analyses of metabolite and transcript data revealed clusters of functionally related metabolites and transcripts active in these different developmental and metabolic programs. The gene clusters provide a resource to generate predictions about the associations and interactions of unknown regulators with their targets based on “guilt-by-association” relationships. The inferred regulators also represent potential targets for future metabolic engineering of relevant pathways and steps in central carbon and nitrogen metabolism in soybean embryos and drought and desiccation tolerance in plants. SUBMITTER_CITATION: Biology 2013, 2(4), 1311-1337; doi:10.3390/biology2041311 Changes in RNA Splicing in Developing Soybean (Glycine max) Embryos Delasa Aghamirzaie, Mahdi Nabiyouni, Yihui Fang, Curtis Klumas, Lenwood S. Heath, Ruth Grene and Eva Collakova SUBMITTER_CITATION: Metabolites 2013, 3(2), 347-372; doi:10.3390/metabo3020347 Metabolic and Transcriptional Reprogramming in Developing Soybean (Glycine max) Embryos Eva Collakova, Delasa Aghamirzaie, Yihui Fang, Curtis Klumas, Farzaneh Tabataba, Akshay Kakumanu, Elijah Myers, Lenwood S. Heath and Ruth Grene Total mRNA profiles of 10 time course samples of Soybean developing embryos with three replicates per sample were generated by deep sequencing, using Illumina HiSeq 2000
Project description:Summary: We build a model for the molecular and cellular events underlying phenotypic discordance in glycine receptor defects (beta subunit). Some mice progress and die, while their littermates recover and get better, despite the same mutation on an inbred genetic background. We find evidence for glycine neurotransmitter toxicity and loss of glycinergic interneurons early in the disease, but some mice are able to keep things going until they can over-express homomeric alpha1 channels, whereupon they recover. In the mice progressing towards lethality, neurotransmitter toxicity too quickly extends to GABAergic interneurons and motorneurons, and they lose their window of time to upregulate the alpha1 glycine receptor, and they crash and burn. Importantly, human patients with glycine receptor defects typically show a resolution of their phenotype with age, and we propose that the same remodeling events are occuring in human patients. Hypothesis: Our data suggests that functional recovery of GlyRb mutant mice is likely due to expression of homomeric glycine receptors, rescue from excitotoxicity, and subsequent neuronal remodeling. We propose that human patients with hyperekplexia (mutations of glycine receptors) show remodeling similar to that of the recovering spastic mice, as human patients also show a lessening of symptoms as a function of age. Specific Aim: Murine models for human Startle Disease show clinical variability between littermates. Here, we determined the molecular remodeling of spastic GlyRb mutant spinal cord through the course of the disease, and develop a model for clinical disparity between littermates. At young ages, all animals were spastic, showed loss of glycine receptors, increased expression of vesicular glycine/GABA transporter and NMDA receptors, induction of activated caspase3, and preferential loss of glycinergic interneurons consistent with neurotransmitter toxicity model. Those littermates that recovered from symptoms showed strong over-expression of the GlyRa1 subunit, and increased myelination and synaptic plasticity. Littermates that showed a deteriorating clinical course failed to over-express GlyRa1, and also showed relative loss of gephyrin. These molecular changes were associated with preferential loss of GABAergic interneurons, and extensive motorneuron loss.