Soybean seeds contain substantial amount of diverse triterpenoid saponins that influence the seed quality, although little is known about the physiologic functions of saponins in plants. We now describe the modification of saponin biosynthesis by RNA interference (RNAi)-mediated gene silencing targeted to β-amyrin synthase, a key enzyme in the synthesis of a common aglycon of soybean saponins. We identified two putative β-amyrin synthase genes in soybean that manifested distinct expression patterns with regard to developmental stage and tissue specificity. Given that one of these genes, GmBAS1, was expressed at a much higher level than the other (GmBAS2) in various tissues including the developing seeds, we constructed two RNAi vectors that encode self-complementary hairpin RNAs corresponding to the distinct regions of GmBAS1 under the control of a seed-specific promoter derived from the soybean gene for the α' subunit of the seed storage protein β-conglycinin. These vectors were introduced independently into soybean. Six independent transgenic lines exhibited a stable reduction in seed saponin content, with the extent of saponin deficiency correlating with the β-amyrin synthase mRNA depletion. Although some transgenic lines produced seeds almost devoid of saponins, no abnormality in their growth was apparent and the antioxidant activity of their seeds was similar to that of control seeds. These results suggest that saponins are not required for seed development and survival, and that soybean seeds may therefore be amenable to the modification of triterpenoid saponin content and composition through molecular biologic approaches.
SummaryThe liver plays the main role in the secretion of food-derived ␣ -tocopherol into the circulation through the functioning of ␣ -tocopherol transfer protein ( ␣ -TTP). However, the effect of liver disease on ␣ -TTP level and ␣ -tocopherol metabolism has not been clarified. We examined the amount of liver ␣ -TTP and its effect on serum ␣ -tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D -galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, ␣ -tocopherol concentrations, and hepatic ␣ -TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic ␣ -TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the ␣ -TTP protein level had begun to decrease. Lipid and ␣ -tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver ␣ -tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic ␣ -TTP synthesis in rats. Serum ␣ -tocopherol concentration was not directly affected by the acute change in hepatic ␣ -TTP level, suggesting that the chronic changes in ␣ -TTP activity would be necessary to regulate serum ␣ -tocopherol concentration.
An 83-year-old man was diagnosed with adult-onset Still's disease (AOSD) based on clinical and laboratory findings. However, glucocorticoid had little effect. Epstein-Barr virus (EBV)-DNA was detected in peripheral blood, and autopsy findings confirmed a diagnosis of chronic active EBV infection (CAEBV). CAEBV mimics AOSD, and the presence of articular involvement and leukocytosis does not exclude the possibility of CAEBV. CAEBV should be included in the differential diagnosis of AOSD, and measurement of EBV-DNA is essential.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.