Project description:Plant roots are the primary site of perception and injury for saline-alkaline stress. The current knowledge of the saline-alkaline stress transcriptome is most focused on salt (NaCl) stress. Only a little alkaline (NaHCO3) stress transcriptome is limited to one time point after stress. Time-course analysis and comparative investigation on roots in the alkaline stress condition are needed to understand the gene response networks that are subject to alkaline tolerance. We used microarrays to detail the global programme of gene expression underlying NaHCO3 treatment and identified distinct classes of regulated genes during this process.
Project description:Plant roots are the primary site of perception and injury for saline-alkaline stress. The current knowledge of the saline-alkaline stress transcriptome is most focused on salt (NaCl) stress. Only a little alkaline (NaHCO3) stress transcriptome is limited to one time point after stress. Time-course analysis and comparative investigation on roots in the alkaline stress condition are needed to understand the gene response networks that are subject to alkaline tolerance. We used microarrays to detail the global programme of gene expression underlying NaHCO3 treatment and identified distinct classes of regulated genes during this process. Three week old Glycine soja seedling roots from 3cm root apex were harvested in two independent biological replicates after 0, 0.5, 1, 3, 6, 12 and 24h treatment with 50mmol/L NaHCO3 stress for RNA extraction and hybridization on Affymetrix microarrays. To minimize biological variance, roots from three plants originating from the same experiment, condition and cultivar was pooled.
Project description:Compositional changes in the microbiota (dysbiosis) may be a basis for Irritable Bowel Syndrome (IBS) but biomarkers are currently unavailable to direct microbiota-directed therapy. We therefore examined whether changes in fecal β-defensin could be a marker of dysbiosis in a murine model. Experimental dysbiosis was induced using four interventions relevant to IBS: a mix of antimicrobials, westernized diets (high-fat/high-sugar and, high salt diets), or mild restraint stress. Fecal mouse β-defensin-3 and 16S rRNA-based microbiome profiles were assessed at baseline, during and following these interventions. Each intervention, except for mild restraint stress, altered compositional and diversity profiles of the microbiota. Exposure to antimicrobials or a high-fat/high-sugar diet, but not mild restraint stress, resulted in decreased fecal β-defensin-3 compared to baseline. In contrast, exposure to the high salt diet increased β-defensin-3 compared to baseline but this was not accompanied by discernible inflammatory changes in the host.
Project description:Mitochondrial rRNAs play important roles in regulating mtDNA-encoded gene expression and energy metabolism subsequently. However, the proteins that regulate mitochondrial 16S rRNA processing remain poorly understood. Herein, we generated adipose-specific Wbscr16-/- mice and cells, both of which exhibited dramatic mitochondrial changes. Subsequently, WBSCR16 was identified as a 16S rRNA-binding protein essential for the cleavage of 16S rRNA-mt-tRNALeu, facilitating 16S rRNA processing and mitochondrial ribosome assembly. Additionally, WBSCR16 recruited RNase P subunit MRPP3 to nascent 16S rRNA and assisted in this specific cleavage. Furthermore, evidence showed that adipose-specific Wbscr16 ablation promotes energy wasting via lipid preference in brown adipose tissue, leading to excess energy expenditure and resistance to obesity. In contrast, overexpression of WBSCR16 upregulated 16S rRNA processing and induced a preference for glucose utilization in both transgenic mouse models and cultured cells. These findings suggest that WBSCR16 plays essential roles in mitochondrial 16S rRNA processing in mammals, and is the key mitochondrial protein to balance glucose and lipid metabolism.