Accumulation of Pyrrolizidine Alkaloids in Benomyl-Treated Tall Fescue Parents and their Untreated Progenies

Both pyrrolizidine alkaloids (N-formyl loline and N-acetyl loline) and the seed-transmitted endophytic fungus tentatively identified as Sphacelia typhina (Pers.) Sacc. (=Acremonium coenophialum Morgan-Jones and W. Gams), the imperfect stage of Epichloe typhina (Fr.) Tul., have been suspected as etiological agents of summer syndrome. Summer syndrome is a toxicological disorder exhibited by cattle grazing tall fescue (Festuca arundinacea Schreb.) under high ambient temperatures. The primary objective of this study was to investigate the relationship between content of N-formyl and N-acetyl loline alkaloids (FALA) and the presence of the endophyte, summer forage yield, moisture content, and acid-detergent fiber in the field. The presence of the endophyte was determined cytologically and FALA were quantified by gas-liquid chromatography. The endophyte was controlled by soil treatment of parent plants in the greenhouse with the systemic fungicide benomyl. Polycross progeny seed were collected and grown out for comparison with parents. Though the endophyte was not eradicated by benomyl, in many parents benomyl impeded infection of the seed, thus reducing transmission of the endophyte to its progenies. In progenies with a lesser degree of endophyte infection than their parents, FALA content of summer forage and seed was likewise lower. These data indicate an association between the endophyte and accumulation of FALA. Correlation coefficients between FALA and summer forage yield, moisture content, and acid-detergent fiber were low, suggesting that selection for FALA would not likely result in correlated responses for these traits. In a follow-up greenhouse experiment, the endophyte and FALA were lost in several plants from one progeny line, indicating that the endophyte and FALA accumulation capacity can be inhibited or eliminated in established plants. Since only one progeny line was involved, this effect may be genotype dependent.