BackgroundTransposable elements (TEs) are prominent features in many plant genomes, and patterns of TEs in closely related rice species are thus proposed as an ideal model to study TEs roles in the context of plant genome evolution. As TEs may contribute to improved rice growth and grain quality, it is of pivotal significance for worldwide food security and biomass production.ResultsWe analyzed three cultivated rice species and their closest five wild relatives for distribution and content of TEs in their genomes. Despite that the three cultivar rice species contained similar copies and more total TEs, their genomes contained much longer TEs as compared to their wild relatives. Notably, TEs were largely depleted from genomic regions that corresponded to genes in the cultivated species, while this was not the case for their wild relatives. Gene ontology and gene homology analyses revealed that while certain genes contained TEs in all the wild species, the closest homologs in the cultivated species were devoid of them. This distribution of TEs is surprising as the cultivated species are more distantly related to each other as compared to their closest wild relative. Hence, cultivated rice species have more similar TE distributions among their genes as compared to their closest wild relatives. We, furthermore, exemplify how genes that are conferring important rice traits can be regulated by TE associations.ConclusionsThis study demonstrate that the cultivation of rice has led to distinct genomic distribution of TEs, and that certain rice traits are closely associated with TE distribution patterns. Hence, the results provide means to better understand TE-dependent rice traits and the potential to genetically engineer rice for better performance.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3454-z) contains supplementary material, which is available to authorized users.

An integrated strategy for complete lignocellulose saccharification to maximize bioethanol yield under a cost-effective and green-like biomass process in rapeseed stalk.

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Glucose converted from a diet has been considered a high risk factor of type 2 diabetes mellitus (T2DM). However, it is not clear how it increases the risk of T2DM. Here, we investigated the effect of high glucose administration on glucose tolerence in wild type and toll like receptor 4 (TLR4) knockout mice. Mice were intragastrically administered with high glucose. The level of fasting blood glucose, insulin and intraperitoneal glucose tolerance were measured, and insulinogenic index and HOMA IR were calculated at 1 week. To understand mechanism of glucose action, we also assessed blood glucose, glucagon like peptide 1 and inflammatory cytokines levels at different time windows following high glucose load. Our results show that 20 g/kg glucose load leads to glucose tolerance impairment and insulin resistance in wild type mice. Following 20 g/kg glucose load, the levels of plasma interlukin 6 (IL 6) and tumor necrosis factor α (TNF α) increased significantly in wild type mice, but not in TLR4 knockout mice. Moreover, 20 g/kg glucose load also impaired glucose induced GLP 1 secretion in wild type and TLR4 knockout mice. Our results indicate that high glucose load leads to glucose intolerance with insulin resistance through impairment of GLP 1 secretion, increase of blood glucose levels via activating TLR4 and increasing levels of IL 6 and TNF α in mice.

FOOD INTAKE results in the secretion of incretin hormones in the body, among which glucagon-like peptide 1 (GLP-1) and glucose-dependent insulin-releasing polypeptide (GIP) are responsible for 50%-70% insulin secretion after a meal [1]. Oral administration of glucose and fat results in two overlapping phases of GLP-1 secretion [2]. The early phase begins within minutes of a meal and continues for 30-60 min. The second phase causes prolonged secretion of GLP-1 at 1-3 h after a meal. This delayed phase of secretion involves the direct detection of luminal contents through enteroendocrine L-cells [1].Dietary nutrients, including carbohydrates, lipids, amino acids, and bile acids, can trigger GLP-1 release from particular intestinal endocrine L-cells. Specifically, glucose is a well-established stimulus for GLP-1 and GIP secretion in vivo. Studies suggested Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum Abstract. Luminal glucose is an important stimulus for glucagon-like peptide 1 (GLP-1) secretion from intestinal endocrine cells. However, the effects of luminal glucose concentration on GLP-1 secretion remain unknown. In this study, we investigated the effect of luminal glucose concentrations (3.5, 5, 10, 15, and 20 mmol/L) on GLP-1 secretion from isolated perfused rat ileum. Results showed that the perfusate glucose concentration dose-dependently stimulated GLP-1 secretion from isolated perfused rat ileum, which was eliminated by the sweet taste receptor inhibitor gurmarin (30 μg/mL), but not inhibited by phloridzin (1 mmol/L), a Na + -coupled glucose transporters inhibitor. We conclude that luminal glucose induced GLP-1 secretion from perfused rat ileum in a concentration-dependent manner. This secretion was mediated by sweet taste receptor transducing signal for GLP-1 release on the gut of rat.

ABSTRACT. Disc degeneration is strongly associated with back or neck pain, sciatica, and disc herniation or prolapse. It places an enormous economic burden on society and can greatly affect quality of life. Alternative treatment approaches, such as genetic therapies, are urgently needed to slow or reverse the disc degeneration process. We downloaded gene expression data from Gene Expression Omnibus during various stages of disc degeneration and identified differentially expressed genes (DEGs) as well as dysfunctional pathways through comparisons with controls. We identified 2 significant DEGs between grade II and III discs and 8 significant DEGs between grade II and IV discs. By constructing an interactive network of the DEGs, we found that mitogen-activated protein family genes and Ras homologous (Rho) family genes -in particular, MAP2K6 and RHOBTB2 -may play important roles in the progression of degeneration of grade III and IV discs, respectively. MAP2K6 and RHOBTB2 may be specific therapeutic molecular targets in the treatment of disc degeneration. However, further experiments are needed to confirm this result.

Aims To investigate the association between two RIG‐I‐like receptor gene polymorphisms and hepatitis C virus (HCV) infection in Chinese Han population. Methods The current study genotyped two selected SNPs (IFIH1 rs3747517 and DDX58 rs9695310) using TaqMan allelic discrimination assay to assess their association with the susceptibility and clinical outcome of HCV infection among 3065 participants (1545 non‐HCV infection individuals, 568 spontaneous HCV clearance cases, and 952 persistent infection patients). Results IFIH1 rs3747517 (dominant model: Adjusted odds ratio [OR] = 1.34, 95% confidence interval [CI] = 1.07‐1.68; P = 0.009) and DDX58 rs9695310 (dominant model: Adjusted OR = 1.43, 95% CI = 1.15‐1.78; P = 0.001) were associated with chronic hepatitis C (CHC). And the risk of CHC increased when people were carrying more unfavorable rs3747517‐GA/AA and rs9695310‐GC/CC genotypes from zero to two with the chronic rates of 56.72%, 59.38%, and 69.01%, respectively (Ptrend < 0.001). Conclusion Genetic variations at IFIH1 rs3747517 and DDX58 rs9695310 were independent predictors of chronic hepatitis C in Chinese Han population.

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