Ontology highlight
ABSTRACT:
PROVIDER: PRJNA639320 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12014700_1.fastq.gz | Fastqsanger.gz | |||
| SRR12014700_2.fastq.gz | Fastqsanger.gz | |||
| SRR12014701_1.fastq.gz | Fastqsanger.gz | |||
| SRR12014701_2.fastq.gz | Fastqsanger.gz | |||
| SRR12014702_1.fastq.gz | Fastqsanger.gz |
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Project description:Energy densification and enrichment of monounsaturated fatty acids increases oat’s nutritional value among small grain cereals. However, optimization of oat oil traits is challenging through conventional breeding. Using the biolistic method for oat’s oil improvement, here we showed that metabolic engineering is a feasible strategy in improving the oil traits of oat. In this study, two constructs containing three genes involved in lipid biosynthesis pathway (AtWRI1, AtDGAT, and SiOLEOSIN) were transformed into oat cultivar ‘Park’ to enhance the oil composition and content in oat grain and leaves. We performed RNA-sequencing in mature seeds and boot leaves of trasngenic lines. Transgene expression contributed to a global transcriptional reprogramming in oat seeds and leaves. Endogenous DGAT, WRI1, and OLEOSIN genes were up regulated while the genes involved in fatty acid biosynthesis expressed in opposite way between oat seeds and leaves. Transcriptomic studies revealed differential gene expression mainly enriched in lipid metabolism.
2024-12-06 | GSE249079 | GEO
Project description:We describe a unique phenotype, blastulation failure, in three primary infertile males with oligoasthenoteratozoospermia (OAT) who underwent intracytoplasmic sperm injection (ICSI), resulting in multiple good-quality cleavage embryos that repeatedly failed to achieve blastulation or implantation. Single-cell analysis revealed that the arrested embryos had complex spermatozoa-derived chromosomal abnormalities, major embryonic genome activation failure, and overactivation of stress and apoptosis pathways at the transcriptional level. We further identified mutations in the meiosis-specific kinetochore factor MEIKIN gene in these males, causing OAT and chromosomal chaos in the spermatozoa. This study is the first to establish a connection between the genetic etiology of OAT and a novel embryo development arrest phenotype, indicating potenial risks of ICSI for OAT patients and providing a new explanation for recurrent implantation failure.
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Project description:Pancreatic ductal adenocarcinoma (PDA) cells have a distinct dependence on de novo ornithine synthesis from glutamine via ornithine aminotransferase (OAT), which supports polyamine synthesis and is required for tumor growth. This directional OAT activity is normally largely restricted to infancy and contrasts with the reliance of most adult normal tissues and other cancer types on arginase (ARG) to generate arginine-derived ornithine, the substrate for polyamine synthesis. This dependence associates with arginine depletion in PDA tumor microenvironment, and is driven by mutant KRAS, which induces the expression of OAT and polyamine synthesis enzymes, including the rate-limiting enzyme ornithine decarboxylase-1 (ODC1). Loss of OAT, but not ARG2, largely mimics loss of ODC1, altering the transcriptional profiles in PDA cells, which in turn correlate with alterations in open chromatin states.
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Project description:The goal was to measure the postprandial effect of an oat bran meal on gene expression in leukocytes from healthy subjects and to investigate the postprandial glucose, insulin and triglyceride responses. Linear mixed models were used for the array data to study the simultaneous dependency on many factors and functional categories of genes whose expression were correlated with oat bran intake were determined.
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Project description:Malignant gliomas are common and aggressive primary brain tumors which are incurable by conventional therapies. Immunotherapy with the immune checkpoint inhibitors is not effective due to the highly immunosuppressive tumor microenvironment (TME). Clinical and experimental data show upregulation of Arginase1 (ARG1) expression in rodent and human malignant gliomas. The elevated ARG1 activity leads to depletion of L-arginine required for proliferation of T lymphocytes and natural killer cells. Inhibition of ARG1 in TME may unblock T cell proliferation and activate effective antitumor responses. To explore an antitumor potential of ARG1 inhibition, first we analyzed bulk and single cell RNA sequencing (scRNA-seq) data from human and murine gliomas, and found upregulation of ARG1 expression in malignant gliomas, both in tumor cells and in tumor infiltrating microglia, monocytes/macrophages. We employed the novel, selective arginase inhibitor - OAT-1746 to interfere with microglia-induced glioma invasion in microglia-glioma co-cultures. We determined its antitumor efficacy as a monotherapy and in combination with immunotherapy. In a Matrigel invasion assay OAT-1746 blocked microglia-dependent invasion of U87-MG and LN18 glioma cells better than reference compounds, without affecting cell viability. OAT-1746 effectively crossed the BBB and increased arginine levels in brains of GL261 glioma bearing mice. The compound reduced glioma growth and increased antitumor effects of the anti-PD-1 antibody. Treatment with OAT-1746 modified TME as demonstrated by profound transcriptomic changes visualized by RNA sequencing. Our findings provide the evidence that inhibition of ARG1 in tumor cells and myeloid cells in TME abolishes the immunosuppressive reprograming of myeloid cells and improves the efficacy of immunotherapy.
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