ABSTRACT
Improvement in nitrogen-use efficiency (NUE) on maize is among the best strategies to mitigate the problems of poor soil fertility in tropical conditions. The objectives of this study were: i) to quantify the genetic variability for NUE-components and agronomic traits in a set of tropical maize inbred lines; ii) to study the genetic divergence among tropical maize inbred lines under contrasting nitrogen (N) levels; iii) to identify the secondary traits associated with NUE in tropical maize inbred lines; and iv) to identify maize inbred lines efficient in NUE and its components. Sixty-four tropical maize inbred lines were evaluated in the field under low- and high-N conditions for NUE-components and agronomic traits. Genetic variability for NUE-components and agronomic traits was found; lines in eight different groups for each N condition were allocated, and N-efficient inbred lines were identified in different groups. Furthermore, we suggest flowering time traits and kernel number as great secondary traits for selecting tropical maize inbred lines for NUE under both N conditions, and chlorophyll content for selecting for NUE under N stress.
Subject(s)
Genotype , Nitrogen/metabolism , Plant Breeding , Polymorphism, Genetic , Quantitative Trait, Heritable , Zea mays/genetics , InbreedingABSTRACT
Hereditary hemochromatosis type 3 is an iron (Fe)-overload disorder caused by mutations in transferrin receptor 2 (TfR2). TfR2 is expressed highly in the liver and regulates Fe metabolism. The aim of this study was to investigate duodenal Fe absorption and hepatic Fe uptake in a TfR2 (Y245X) mutant mouse model of hereditary hemochromatosis type 3. Duodenal Fe absorption and hepatic Fe uptake were measured in vivo by 59Fe-labeled ascorbate in TfR2 mutant mice, wild-type mice, and Fe-loaded wild-type mice (2% dietary carbonyl Fe). Gene expression was measured by real-time RT-PCR. Liver nonheme Fe concentration increased progressively with age in TfR2 mutant mice compared with wild-type mice. Fe absorption (both duodenal Fe uptake and transfer) was increased in TfR2 mutant mice compared with wild-type mice. Likewise, expression of genes participating in duodenal Fe uptake (Dcytb, DMT1) and transfer (ferroportin) were increased in TfR2 mutant mice. Nearly all of the absorbed Fe was taken up rapidly by the liver. Despite hepatic Fe loading, hepcidin expression was decreased in TfR2 mutant mice compared with wild-type mice. Even when compared with Fe-loaded wild-type mice, TfR2 mutant mice had increased Fe absorption, increased duodenal Fe transport gene expression, increased liver Fe uptake, and decreased liver hepcidin expression. In conclusion, despite systemic Fe loading, Fe absorption and liver Fe uptake were increased in TfR2 mutant mice in association with decreased expression of hepcidin. These findings support a model in which TfR2 is a sensor of Fe status and regulates duodenal Fe absorption and liver Fe uptake.
Subject(s)
Duodenum/metabolism , Hemochromatosis/genetics , Intestinal Absorption , Iron/metabolism , Liver/metabolism , Receptors, Transferrin/genetics , Animals , Base Sequence , Biological Transport , Crosses, Genetic , DNA Primers , Disease Models, Animal , Female , Ferritins/metabolism , Genetic Carrier Screening , Hemochromatosis/metabolism , Iron/blood , Male , Mice , Mice, Inbred C57BL , Mice, Mutant StrainsABSTRACT
We describe a patient with arteriovenous shunting during renal arteriography who at operation was found to have an angiomyolipoma rather than renal cell carcinoma or an arteriovenous malformation. Renal angiomyolipoma should be added to the list of causes of gross hematuria with angiographically demonstrable arteriovenous shunting.
