Metabolites of plants and their role in resistance to phytopathogens

Plant disease resistance is a complex reaction where biochemical peculiarities play a major role. The review is focused on two strategies of improvement of plant resistance to some groups of pathogens. The first strategy is based on a dependence of pathogens on certain plant compounds, i.e. sterols. The lack of these metabolites in a host plant repress pathogen development and reproduction. Here we present modern data on sterol metabolism and their functions in plants as well as description of known plant sterol mutants. The other way to improve plant resistance is to stimulate biosynthesis of secondary metabolites with antimicrobial activity. The roles of phytoalexins and steroid glycoalcoloids in the development of plant resistance is described here on certain examples

Azasterol inhibitors in yeast. Inhibition of the Δ24-sterol methyltransferase and the 24-methylene sterol Δ24(28)-reductase in sterol mutants of Saccharomyces cerevisiae

The effects of several monoazasterols on sterol biosynthesis were examined in the ergosterol deficient mutants erg 2, erg 3, and erg 5 of Saccharomyces cerevisiae. When the mutants were aerobically cultured in the presence of 1 μM 23-azacholesterol, the 24-methylene sterol Δ24(28)-reductase was essentially blocked and the immediate Δ24(28)-unsaturated precursor of the final sterol metabolite in each respective erg strain was found to accumulate. Total sterol production was enhanced in the cultures grown in the presence of 1 μM 23-azacholesterol. In cultures which were grown in the presence of 1 μM 25-azacholesterol which effectively blocked the Δ24-sterol methyltransferase, all three erg strains accumulated zymosterol as the major sterol component with lesser quantities of predicted terminal sterols. Mutant erg 2 (block at Δ8 → Δ7 isomerase) grew poorly in the presence of 1 μM 25-azacholesterol and produced low levels of cholesta-5,8,24-trienol and cholesta-5,8,22,24-tetraenol, which were isolated and characterized for the first time. Compared with controls, erg 2 treated with 1 μM 23-azacholesterol produced increased amounts of ergosta-5,8,22,24(28)-tetraenol, which was hitherto unidentified as a yeast sterol. In erg 5 (block at Δ22-dehydrogenase) treatment with 1 μM 25-azacholestanol effectively blocked the Δ24-sterol methyltransferase and resulted in increased total sterol production. Cholesta-5,7,24-trienol accounted for 27–29% of the sterol pool in 25-azasterol inhibited erg 5 cultures. The 25-azasteroi inhibited erg 5 mutant thus provides a source of cholesta-5,7,24-trienol, a potential provitamin D3 substitute.