Endogenous cytokinins in Cocos nucifera L. in vitro cultures obtained from plumular explants.

Auxin induces in vitro somatic embryogenesis in coconut plumular explants through callus formation. Embryogenic calli and non-embryogenic calli can be formed from the initial calli. Analysis of endogenous cytokinins showed the occurrence of cytokinins with aromatic and aliphatic side chains. Fourteen aliphatic cytokinins and four aromatic cytokinins were analysed in the three types of calli and all the cytokinins were found in each type, although some in larger proportions than others. The most abundant cytokinins in each type of callus were isopentenyladenine-9-glucoside, zeatin-9-glucoside, zeatin riboside, isopentenyladenine riboside, dihydrozeatin and dihydrozeatin riboside in decreasing order. Total cytokinin content was compared between the three types of calli, and it was found to be lower in embryogenic calli compared to non-embryogenic calli or initial calli. The same pattern was observed for individual cytokinins. When explants were cultured in media containing exogenously added cytokinins, the formation of embryogenic calli in the explants was reduced. When 8-azaadenine (an anticytokinin) was added the formation of embryogenic calli and somatic embryos was increased. These results suggest that the difference in somatic embryo formation capacity observed between embryogenic calli and non-embryogenic calli is related to their endogenous cytokinin contents.

Familial hypercholesterolemia: mechanism of inheritance.

We have studied a large family of 95 members with a defect in the metabolism of cholesterol, which is transmitted through three generations. The following characteristics of the family support the classification of the disorder as familial hypercholesterolemia : hypercholesterolemia, increased levels of phospholipids an beta-lipoproteins, normal values of triglycerides, pre-beta-lipoproteins and blood sugar, xanthomas, xanthelasmas, corneal arcus and early appearance of ischemic heart disease. Segregation analyses of the hypercholesterolemia and the findings of a bimodal distribution of total plasma cholesterol in the family suggest a monogenic autosomal dominant mechanism of transmission of this lipid disorder.