An embryo lethal transgenic line manifests global expression changes and elevated protein/oil ratios in heterozygous soybean plants
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA540437 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Understanding the molecular processes of seed development is important especially in agronomic crops that produce large amounts of nutrient reserves. Because soybean is a vital source of vegetable protein worldwide, producers are concerned about increasing the total amount of protein in the seed without substantially lowering the amount of oil, another economically important product. Here we describe a transgenic soybean line with increased protein and protein/oil ratio, containing an average of 42.2% protein vs. 38.5% in controls and with a protein/oil ratio of 2.02 vs. 1.76 in controls over several generations of greenhouse growth. Other phenotypic data show that the seeds are heavier, although there are overall lower yields per plant. We postulate these effects result from insertion site mutagenesis by the transgenic construct. As this line never achieves homozygosity and appears to be embryo lethal when homozygous, one functional copy of the gene is most likely essential for normal seed development. Global transcript analyses using RNA-Seq for 88,000 gene models over two stages of cotyledon development revealed that more genes are over-expressed in the transgenic line including ribosomal protein related genes and those in the membrane protein and transporters families. Localization of the insertion site should reveal the genes and developmental program that has been perturbed by the transgenic construct, resulting in this economically interesting increase in protein and the protein/oil ratio.
2020-06-10 | GSE130483 | GEO
Project description:Understanding the molecular processes of seed development is important especially in agronomic crops that produce large amounts of nutrient reserves. Because soybean is a vital source of vegetable protein worldwide, producers are concerned about increasing the total amount of protein in the seed without substantially lowering the amount of oil, another economically important product. Here we describe a transgenic soybean line with increased protein and protein/oil ratio, containing an average of 42.2% protein vs. 38.5% in controls and with a protein/oil ratio of 2.02 vs. 1.76 in controls over several generations of greenhouse growth. Other phenotypic data show that the seeds are heavier, although there are overall lower yields per plant. We postulate these effects result from insertion site mutagenesis by the transgenic construct. As this line never achieves homozygosity and appears to be embryo lethal when homozygous, one functional copy of the gene is most likely essential for normal seed development. Global transcript analyses using RNA-Seq for 88,000 gene models over two stages of cotyledon development revealed that more genes are over-expressed in the transgenic line including ribosomal protein related genes and those in the membrane protein and transporters families. Localization of the insertion site should reveal the genes and developmental program that has been perturbed by the transgenic construct, resulting in this economically interesting increase in protein and the protein/oil ratio.
| S-EPMC7282645 | biostudies-literature
Project description:YY1-dependent transcriptional regulation manifests at the morula stage
| PRJNA1057211 | ENA
Project description:STING-Dependent Signaling Manifests IL-10 Controlled Inflammatory Colitis
| PRJNA421445 | ENA
Project description:Goal of the experiment: To examine differential gene expression in the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice treated with vehicle or pioglitazone. Brief description of the experiment: The objective of this study was to use whole mouse genome DNA microarrays (Codelink) to examine gene expression the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice. Women with polycystic ovary syndrome (PCOS) treated with thiazolidinediones (TZD), such as pioglitazone, show reduced androgen levels and improved ovulatory function. Recent evidence suggests that TZD, acting via peroxisome proliferator-activated receptor gamma (PPAR gamma), alter the expression of ovarian genes involved in insulin/IGF signaling that may account for some of the observed effects. Since TZD can alter the expression of a large variety of genes, there may be other mechanisms involved in the improvement of ovarian function with TZD treatment. Lethal yellow (LY) mice exhibit progressive obesity, reproductive dysfunction, and altered metabolic regulation (e.g. insulin and leptin resistance) similar to women with PCOS. This study was designed to test the hypothesis that prolonged treatment of aging LY mice with pioglitazone would alter the expression of ovarian genes involved in reproduction. Beginning at 120-days and continuing until 180-days of age, female LY mice received daily oral doses of either 0.1 mg pioglitazone (n = 4) or an equal volume of vehicle (0.1 ml 100% DMSO; n = 4). At the end of the treatment regimen, ovaries were removed and RNA extracted. Total RNA extracts were run individually on Codelink Mouse Whole Genome Bioarrays (GE). Relative gene expression was compared between treatments by t-test using GeneSpring software. Keywords: mouse, drug treatment Experimental factors: drug treatment Keywords: drug treatment
2008-07-08 | GSE8806 | GEO
Project description:Vascular Surgery Patients with Elevated Neutrophil Lymphocyte Ratios Have Downregulated Neutrophil Complement RNA Expression
| PRJNA869449 | ENA
Project description:Experiments were performed to investigate the BAT proteome of RNF20 WT and heterozygous-null mice.
2024-02-05 | PXD048556 | Pride
Project description:Identification of biological processes that distinguish lethal from non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity to during lethal influenza infection. For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology.
2013-07-03 | GSE42638 | GEO
Project description:Identification of biological processes that distinguish lethal from non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity to during lethal influenza infection. For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology. Multiple mice were either sham infected, infected with the seasonal H1N1 influenza A virus TX91 (10^6PFU), or infected with various sublethal or lethal doses of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at various time points (24h, 48h, 72h and 240h post infection) and processed to yield whole lung RNA that was used for microarray analysis. The dataset contains 138 microarrays covering 20 experimental conditions with 7 biological replicates each. As an exception, the alternative non-infectious control condition (Alum treatment) contains 5 biological replicates. This dataset is linked to a dataset comparing the transcriptomes of 5 different cell types isolated from individual lungs of influenza A-infected or control animals (contains 75 microarrays covering 25 experimental conditions).
2013-07-03 | E-GEOD-42638 | biostudies-arrayexpress
Project description:Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection. For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology.
2013-07-03 | GSE42639 | GEO