Salinity affects more than 6% of the world's total land area, causing massive losses in crop yield. Salinity inhibits plant growth and development through osmotic and ionic stresses; however, some plants exhibit adaptations through osmotic regulation, exclusion, and translocation of accumulated Na+ or Cl-. Currently, there are no practical, economically viable methods for managing salinity, so the best practice is to grow crops with improved tolerance. Germination is the stage in a plant's life cycle most adversely affected by salinity. Barley, the fourth most important cereal crop in the world, has outstanding salinity tolerance, relative to other cereal crops. Here, we review the genetics of salinity tolerance in barley during germination by summarizing reported quantitative trait loci (QTLs) and functional genes. The homologs of candidate genes for salinity tolerance in Arabidopsis, soybean, maize, wheat, and rice have been blasted and mapped on the barley reference genome. The genetic diversity of three reported functional gene families for salt tolerance during barley germination, namely dehydration-responsive element-binding (DREB) protein, somatic embryogenesis receptor-like kinase and aquaporin genes, is discussed. While all three gene families show great diversity in most plant species, the DREB gene family is more diverse in barley than in wheat and rice. Further to this review, a convenient method for screening for salinity tolerance at germination is needed, and the mechanisms of action of the genes involved in salt tolerance need to be identified, validated, and transferred to commercial cultivars for field production in saline soil.
Gene Expression Regulation, Plant ; Genetic Variation ; Germination/physiology* ; Hordeum/physiology* ; Salt Tolerance/genetics*

Fusarium head blight (FHB) caused by Fusarium graminearum is a devastating disease that results in extensive yield losses to wheat and barley. A green fluorescent protein (GFP) expressing plasmid pRP22-GFP was constructed for monitoring the colonization of two biocontrol agents, Brevibacillus brevis ZJY-1 and Bacillus subtilis ZJY-116, on the spikes of barley and their effect on suppression of FHB. Survival and colonization of the Brevibacillus brevis ZJY-1 and Bacillus subtilis ZJY-116 strains on spikes of barley were observed by tracking the bacterial transformants with GFP expression. Our field study revealed that plasmid pRP22-GFP was stably maintained in the bacterial strains without selective pressure. The retrieved GFP-tagged strains showed that the bacterial population fluctuation accorded with that of the rain events. Furthermore, both biocontrol strains gave significant protection against FHB on spikes of barley in fields. The greater suppression of barley FHB disease was resulted from the treatment of barley spikes with biocontrol agents before inoculation with F. graminearum.
Bacillus ; classification ; cytology ; isolation & purification ; physiology ; Cell Survival ; physiology ; Fusarium ; isolation & purification ; pathogenicity ; physiology ; Hordeum ; microbiology ; parasitology ; Pest Control, Biological ; methods ; Plant Diseases ; microbiology ; parasitology ; Species Specificity ; Survival Analysis

OBJECTIVE: We aimed to explore how fermented barley extracts with Lactobacillus plantarum dy-1 (LFBE) affected the browning in adipocytes and obese rats. METHODS: In vitro, 3T3-L1 cells were induced by LFBE, raw barley extraction (RBE) and polyphenol compounds (PC) from LFBE to evaluate the adipocyte differentiation. In vivo, obese SD rats induced by high fat diet (HFD) were randomly divided into three groups treated with oral gavage: (a) normal control diet with distilled water, (b) HFD with distilled water, (c) HFD with 800 mg LFBE/kg body weight (bw). RESULTS: In vitro, LFBE and the PC in the extraction significantly inhibited adipogenesis and potentiated browning of 3T3-L1 preadipocytes, rather than RBE. In vivo, we observed remarkable decreases in the body weight, serum lipid levels, white adipose tissue (WAT) weights and cell sizes of brown adipose tissues (BAT) in the LFBE group after 10 weeks. LFBE group could gain more mass of interscapular BAT (IBAT) and promote the dehydrogenase activity in the mitochondria. And LFBE may potentiate process of the IBAT thermogenesis and epididymis adipose tissue (EAT) browning via activating the uncoupling protein 1 (UCP1)-dependent mechanism to suppress the obesity. CONCLUSION These results demonstrated that LFBE decreased obesity partly by increasing the BAT mass and the energy expenditure by activating BAT thermogenesis and WAT browning in a UCP1-dependent mechanism.
3T3 Cells ; Adipocytes ; drug effects ; physiology ; Adipose Tissue, Brown ; drug effects ; physiology ; Adipose Tissue, White ; drug effects ; physiology ; Animal Feed ; analysis ; Animals ; Anti-Obesity Agents ; administration & dosage ; metabolism ; Cell Differentiation ; drug effects ; Diet ; Fermentation ; Hordeum ; chemistry ; Lactobacillus plantarum ; chemistry ; Male ; Mice ; Obesity ; drug therapy ; genetics ; Plant Extracts ; chemistry ; Probiotics ; administration & dosage ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Uncoupling Protein 1 ; genetics ; metabolism