Brown planthopper (BPH) is a phloem sap-sucking insect pest of rice which causes severe yield loss. We cloned the BPH18 gene from the BPH-resistant introgression line derived from the wild rice species Oryza australiensis. Map-based cloning and complementation test revealed that the BPH18 encodes CC-NBS-NBS-LRR protein. BPH18 has two NBS domains, unlike the typical NBS-LRR proteins. The BPH18 promoter::GUS transgenic plants exhibited strong GUS expression in the vascular bundles of the leaf sheath, especially in phloem cells where the BPH attacks. The BPH18 proteins were widely localized to the endo-membranes in a cell, including the endoplasmic reticulum, Golgi apparatus, trans-Golgi network, and prevacuolar compartments, suggesting that BPH18 may recognize the BPH invasion at endo-membranes in phloem cells. Whole genome sequencing of the near-isogenic lines (NILs), NIL-BPH18 and NIL-BPH26, revealed that BPH18 located at the same locus of BPH26. However, these two genes have remarkable sequence differences and the independent NILs showed differential BPH resistance with different expression patterns of plant defense-related genes, indicating that BPH18 and BPH26 are functionally different alleles. These findings would facilitate elucidation of the molecular mechanism of BPH resistance and the identified novel alleles to fast track breeding BPH resistant rice cultivars.

Summary• In higher plants, the plastidic glucose translocator (pGlcT) is assumed to play a role in the export of starch degradation products, but this has not yet been studied in detail.• To elucidate the role of pGlcT in the leaves of Arabidopsis thaliana, we generated single and double mutants lacking three plastidic sugar transporters, pGlcT, the triose-phosphate ⁄ phosphate translocator (TPT), and the maltose transporter (MEX1), and analyzed their growth phenotypes, photosynthetic properties and metabolite contents.• In contrast to the pglct-1 and pglct-2 single mutants lacking a visible growth phenotype, the double mutants pglct-1 ⁄ mex1 and tpt-2 ⁄ mex1 displayed markedly inhibited plant growth. Notably, pglct-1 ⁄ mex1 exhibited more severe growth retardation than that seen for the other mutants. In parallel, the most severe reductions in sucrose content and starch turnover were observed in the pglct-1 ⁄ mex1 mutant. The concurrent loss of pGlcT and MEX1 also resulted in severely reduced photosynthetic activities and extreme chloroplast abnormalities.• These findings suggest that pGlcT, together with MEX1, contributes significantly to the export of starch degradation products from chloroplasts in A. thaliana leaves, and that this starch-mediated pathway for photoassimilate export via pGlcT and MEX1 is essential for the growth and development of A. thaliana.

A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. Gastric cancer is the second most common cause of cancerrelated death in the world. 1 In Korea, gastric cancer is the most frequently diagnosed malignancy, although the associated mortality rate has been decreasing slowly for the past 10 years. 2 About 60% of Korean adults are infected with Helicobacter pylori. 3,4 Such infection is a causative factor in gastric carcinogenesis, and H. pylori infection is associated with a 2-fold increased risk of developing gastric adenocarcinoma. 5,6 A positive family history is also associated with an increased risk of gastric cancer. 7-10 The possible causes of familial aggregation of gastric cancer are common genetic backgrounds and common environmental risk factors including H. pylori infection, excessive intake of salt and N-nitroso compounds and a deficiency of dietary antioxidants among patients with gastric cancer and their family members. Among these risk factors, intrafamilial clustering of H. pylori infection is regarded as a leading cause of gastric carcinogenesis. This association is significantly greater for H. pylori strains that possess the cytotoxin-associated gene cagA, [11][12][13] a key gene of the so-called "pathogenicity island". 14 The first aim of our study was to examine the prevalence of H. pylori infection in offspring and siblings of patients with gastric cancer to evaluate its role in intrafamilial aggregation of gastric cancer. The second aim was to investigate the relationship between CagA or vacuolating cytotoxin (VacA) seropositivity as virulence markers of H. pylori strains and H. pylori infection in relatives of cancer patients. Finally, we examined the frequency of gastric precancerous lesion, atrophic gastritis and/or intestinal metaplasia in the H. pyloriinfected relatives of cancer patients. MATERIAL AND METHODS Recruitment of relatives of cancer patients and controlsFrom November 2000 to March 2002, we recruited subjects who wished to receive routine upper gastrointestinal endoscopy and evaluation ...

Pyrophosphate: fructose-6-phosphate 1-phosphotransferase (PFP) catalyzes the reversible interconversion of fructose-6-phosphate and fructose-1,6-bisphosphate, a key step in the regulation of the metabolic flux toward glycolysis or gluconeogenesis. To examine the role of PFP in plant growth, we have generated transgenic Arabidopsis plants that either overexpress or repress Arabidopsis PFP sub-unit genes. The overexpressing lines displayed increased PFP activity and slightly faster growth relative to wild type plants, although their photosynthetic activities and the levels of metabolites appeared not to have significantly changed. In contrast, the RNAi lines showed significantly retarded growth in parallel with the reduced PFP activity. Analysis of photosynthetic activity revealed that the growth retardation phenotype of the RNAi lines was accompanied by the reduced rates of CO(2) assimilation. Microarray analysis of our transgenic plants further revealed that the altered expression of AtPFPbeta affects the expression of several genes involved in diverse physiological processes. Our current data thus suggest that PFP is important in carbohydrate metabolism and other cellular processes.