Project description:The global emergence of soil salinization poses a serious challenge to many countries and regions. γ-Aminobutyric acid (GABA) is involved in systemic regulation of plant adaptation to salt stress, but the underling molecular and metabolic mechanism still remains largely unknown. The elevated endogenous GABA level by exogenous application of GABA could significantly improve salt tolerance in creeping bentgrass with the enhancement of antioxidant capacity, photosynthetic characteristics, osmotic adjustment (OA), and water use efficiency. GABA strongly upregulated transcript levels of AsPPa2, AsATPaB2, AsNHX2/4/6, and AsSOS1/20 in roots involved in enhanced capacity of Na+ compartmentalization and mitigation of Na+ toxicity in cytosol. Significant downregulation of AsHKT1/4 expression could be induced by GABA in leaves in relation to maintenance of significantly lower Na+ accumulation and higher K+/Na+ ratio. GABA-depressed aquaporins (AQPs) expression and accumulation induced declines in stomatal conductance and transpiration, thereby reducing water loss in leaves during salt stress. For metabolic regulation, GABA primarily enhanced sugars and amino acids accumulation and metabolism largely contributing to improved salt tolerance through maintaining OA and metabolic homeostasis. Other major pathways could be responsible for GABA-induced salt tolerance including increases in antioxidant defense, heat shock proteins, dehydrins, and myo-inositol accumulation in leaves. Integrative analyses of molecular, protein, metabolic, and physiological changes reveal systemic function of GABA on regulating ions, water, and metabolic homeostasis in non-halophytic creeping bentgrass under salt stress.
2020-01-13 | PXD015066 | Pride
Project description:Transcriptome profiling of creeping bentgrass under drought stress
| PRJNA957937 | ENA
Project description:Transcriptomic analysis of HSP26.8 transgenic and wild type of creeping bentgrass
| PRJNA666285 | ENA
Project description:Adult social environment interacts with sex and age to influence the microbiome in Drosophila melanogaster
Project description:Aging is associated with declining immunity and inflammation as well as alterations in the gut microbiome with a decrease of beneficial microbes and increase in pathogenic ones. The aim of this study was to investigate aging associated gut microbiome in relation to immunologic and metabolic profile in a non-human primate (NHP) model. 12 old (age>18 years) and 4 young (age 3-6 years) Rhesus macaques were included in this study. Immune cell subsets were characterized in PBMC by flow cytometry and plasma cytokines levels were determined by bead based multiplex cytokine analysis. Stool samples were collected by ileal loop and investigated for microbiome analysis by shotgun metagenomics. Serum, gut microbial lysate and microbe-free fecal extract were subjected to metabolomic analysis by mass-spectrometry. Our results showed that the old animals exhibited higher inflammatory biomarkers in plasma and lower CD4 T cells with altered distribution of naïve and memory T cell maturation subsets. The gut microbiome in old animals had higher abundance of Archaeal and Proteobacterial species and lower Firmicutes than the young. Significant enrichment of metabolites that contribute to inflammatory and cytotoxic pathways was observed in serum and feces of old animals compared to the young. We conclude that aging NHP undergo immunosenescence and age associated alterations in the gut microbiome that has a distinct metabolic profile.
Project description:The gastrointestinal ecosystem is a highly complex environment with a profound influence on human health. Inflammation in the gut, linked to an altered gut microbiome has been associated with the development of multiple human conditions including type 1 diabetes (T1D). Viruses infecting the gastrointestinal tract, especially enteroviruses, are also thought to play an important role in T1D pathogenesis possibly via overlapping mechanisms. Here, we apply an integrative approach to combine comprehensive faecal virome, microbiome and metaproteome data sampled before and at the onset of islet autoimmunity in 40 children. We show strong age and antibody related effects across the datasets. Mastadenovirus infection was associated with profound functional changes in the faecal metaproteome. Multiomic factor analysis modelling revealed proteins associated with carbohydrate transport from the genus Faecalibacterium were associated with islet autoimmunity. These findings demonstrate functional remodelling of the gut microbiota accompanies both islet autoimmunity and viral infection.
Project description:In Crohn's disease, creeping fat is the characteristic expansion of mesenteric adipose tissue wrapping around the inflamed intestine. Through a comparative transcriptomic analysis of creeping fat and normal-looking mesenteric adipose tissues from patients with Crohn's disease and non-Crohn's disease, we found that a dynamic transcriptional and cell compositional change occurs during the progression from non-Crohn's disease to Crohn's disease, and finally to creeping fat.
Project description:The gut microbiome shapes local and systemic immunity. The liver is presumed to be a protected sterile site. As such, a hepatic microbiome has not been examined. Here, we show that the liver hosts a robust microbiome in mice and humans that is distinct from the gut and is enriched in Proteobacteria. It undergoes dynamic alterations with age and is influenced by the environment and host physiology. Fecal microbial transfer experiments revealed that the liver microbiome is populated from the gut in a highly selective manner. Hepatic immunity is dependent on the microbiome, specifically Bacteroidetes species. Targeting Bacteroidetes with oral antibiotics reduced the hepatic immune cell infiltrate by ~90%, prevented APC maturation, and mitigated adaptive immunity. Mechanistically, presentation of Bacteroidetes-derived glycosphingolipids to NKT cells promotes CCL5 signaling, which drives hepatic leukocyte expansion and maturation. Collectively, we reveal a microbial – glycosphingolipid – NKT – CCL5 axis that underlies hepatic immunity.