Cucumber is a model cucurbitaceous plant with a known genome sequence which is important for studying molecular mechanisms of root development. In this study, RNA sequencing was employed to explore the mechanism of melatonin-induced lateral root formation in cucumber under salt stress. Three groups of seeds were examined, that is, seeds primed without melatonin (CK), seeds primed in a solution containing 10 or 500 μmol/L melatonin (M10 and M500, respectively). These seeds were then germinated in NaCl solution. The RNA-seq analysis generated 16,866,670 sequence reads aligned with 17,920 genes, which provided abundant data for the analysis of lateral root formation. A total of 17,552, 17,450, and 17,393 genes were identified from roots of the three treatments (CK, M10 and M500, respectively). The expression of 121 genes was significantly up-regulated, and 196 genes were significantly down-regulated in M500 which showed an obvious increase on the number of lateral roots. These genes were significantly enriched in 57 KEGG pathways and 16 GO terms (M500 versus CK). Based on their expression pattern, peroxidase-related genes were selected as the candidates to be involved in the melatonin response. Several transcription factor families might play important roles in lateral root formation processes. A number of genes related to cell wall formation, carbohydrate metabolic processes, oxidation/reduction processes, and catalytic activity also showed different expression patterns as a result of melatonin treatments. This RNA-sequencing study will enable the scientific community to better define the molecular processes that affect lateral root formation in response to melatonin treatment.

The orexigenic hormone ghrelin is a 28-amino-acid peptide derived from a 99-amino-acid precursor and acylated at Ser-3, which was initially isolated from rat stomach. In addition to stimulating appetite and growth, it also plays various important roles in energy homeostasis and in the cardiovascular and immune systems. Although analysis of its physiological effects has yielded many significant results, much less information is available on its biosynthesis and the mechanism of its acylation. In this report, we have studied the endoproteolytic processing of this molecule from its precursor (proghrelin) into mature ghrelin in various prohormone convertase null mouse strains generated in our laboratory and have identified the convertase responsible for this event. Using Western blotting, mass spectrometry, and immunocytochemical methods, we have demonstrated that (a) in mouse stomach, prohormone convertase 1/3 (PC1/3) is the endoprotease responsible for the conversion of proghrelin to ghrelin, (b) the acylation of this peptide is processing-independent, and (c) the expression of proghrelin mRNA is increased in the processing-deficient (PC1/3 null) mouse.Ghrelin, a 28-amino-acid peptide, was initially isolated from rat stomach (1) as a ligand of the growth hormone secretagogue receptor (2). Subsequent studies have revealed that it is a potent orexigenic peptide (3). It is also involved in various functions of the heart (4), pancreatic islets, and insulin secretion (5-10) and also in insulin signaling (11), adipose tissue (12), and the immune system (13). The expression of ghrelin is not limited to the stomach. The duodenum also produces large amounts of ghrelin, and it is also expressed at lower levels in other tissues, such as pancreas, brain, liver, and lung, (14).Similar to many other peptide hormones, ghrelin is processed from a 94-amino-acid precursor. Octanoylation at a serine residue (Ser-3) is necessary for its action via the growth hormone secretagogue receptor, although the desoctanoyl peptide may have alternative functions (15). Interestingly, recent research has revealed another bioactive peptide named obestatin within the ghrelin precursor (16). Obestatin is a 23-amino-acid peptide and is a cognate ligand for receptor GPR39, which is a member of a ghrelin receptor subfamily (17, 18). Although derived from the same precursor, in contrast to the effects of ghrelin, obestatin suppresses food intake, inhibits intestinal activity, and decreases weight gain (16). It is well established that many bioactive peptide hormones are generated by limited proteolytic processing by members of a secretory pathway-specialized serine protease family related to yeast Kex2 (the subtilisin-like prohormone convertase family SPCs or PCs), which includes PC1/3, PC2, and PC5/6A (19,20). Much data has accumulated over the past few years on functional aspects of ghrelin. However, biosynthetic studies have been lacking. In this report, we investigate the processing of proghrelin in various prohormone convertase-deficient mouse mode...

Hepatitis B virus (HBV) is a major risk factor for the development and progression of hepatocellular carcinoma (HCC). It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Here, we report that decreasing levels of the expression of the miRNA miR-192-3p is associated with rising levels of HBV DNA in the serum of HBV patients. We revealed that HBV infection repressed the expression of miR-192-3p through HBx interaction with c-Myc. We further showed that miR-192-3p was repressed by HBV transfection in vitro and in mouse model, leading to cellular autophagy. Using an miRNA target prediction database miRBase, we identified XIAP as a novel target gene of miR-192-3p and demonstrated that miR-192-3p directly targeted XIAP 3'-untranslated region (3'-UTR) of XIAP mRNA. Importantly, we discovered that HBV promoted autophagy through miR-192-3p-XIAP axis and that this process was important for HBV replication in vitro and in vivo. We demonstrated that miR-192-3p functioned through the NF-κB signaling pathway to inhibit autophagy, thereby reducing HBV replication. Our findings indicate that miR-192-3p is a novel regulator of HBV infection and may play a potential role in HCC. It may also serve as a new biomarker or therapeutic target for HBV patients. This article is protected by copyright. All rights reserved.

␤ cell failure is a common denominator of diabetes. Susceptibility to stress-induced apoptosis may underlie ␤ cell failure and͞or hamper islet transplantation therapy. The causal basis is not well understood. In efforts to identify important differences in gene expression in ␣ vs. ␤ cells, a gene termed HIMP1 (Hypoglycemia͞ hypoxia Inducible Mitochondrial Protein, or HIG1) has been cloned from an ␣ cell cDNA library. It is a member of a well conserved eukaryote protein family. In mice, its two alternatively spliced products each form a transmembrane loop, having an NoutsideCoutside orientation and are expressed highly in the mitochondrial inner membrane in several tissues including heart and pancreatic ␣ cells, but not in ␤ cells. Ectopic expression of HIMP1 in MIN6 ␤ cells protects the cells from apoptosis induced by several stimuli and prolongs their survival. These results suggest an important role for HIMP1 in stress protective programs in mitochondria.islet ͉ apoptosis ͉ inner membrane protein ͉ stress D iabetes, including two main types, is one of the most important health problems in the world today. In type 1 diabetes, ␤ cells have been long-recognized to be especially sensitive to various noxious stimuli and also selectively prone to autoimmune destruction. In type 2 diabetes, accumulated findings illustrate that ␤ cell mass is reduced (1-5). However, there is general agreement that an absolute or relative deficiency of insulin is a typical manifestation of this disease and is due to selective loss of ␤ cell mass, often accompanied by elevated production and secretion of glucagon by an increased proportion of ␣ cells. Functional disturbances of pancreatic ␤ and͞or ␣ cells are thus central to the failure to maintain physiological glucose levels and the related metabolic concomitants of this disease.In both types of diabetes, increasing ␤ cell apoptosis is suggested to be mainly responsible for the reduction of ␤ cell mass (6-7). The primary reason for the apoptotic susceptibility of ␤ cells compared to other cell types remains unclear. Is it a cell type-specific property acquired inherently during differentiation due to the attenuation of some beneficial genes, and͞or the turning on of detrimental genes? Or is it due to overloading the ␤ cells under stressful conditions such as hyperglycemia or obesity and their concomitant toxic byproducts such as hydrogen peroxide? Albeit data supporting both views exist, increasing evidence tends to support the former notion because it has been observed that ␤ cells are more sensitive to various apoptotic stimuli, such as the stress of low glucose (8, 9) or hypoxia (10), and ␤ cell apoptosis increases during chronic hyperglycemic conditions (3,(11)(12)(13)(14). The maturation of ␤ cells has also been shown to link to increases in their sensitivity to the apoptotic stimuli of toxins and cytokines (15). In addition, low expression level of various protective genes against oxidative stress, such as catalase, in the ␤ cells has been proposed to contribute to the apoptotic...