Ethylene-Induced Chlorosis in the Pathogenesis of Bipolaris sorokiniana Leaf Spot of Poa pratensis

Endogenous ethylene of Poa pratensis leaves infected by Bipolaris sorokiniana was evaluated as a factor in leaf chlorosis during pathogenesis. Detectable increases in endogenous ethylene of leaves of intact plants under normal ambient pressure occurred 12 hours after inoculation and was maximum at 48 hours; from 48 to 96 hours the ethylene progressively decreased. Necrotic lesions surrounded by chlorotic halos occurred on infected leaves between 24 and 48 hours. Midvein chlorosis interconnecting individual lesions and complete chlorosis of all tissues not directly affected by the lesions occurred between 72 and 96 hours, after maximum production of ethylene at 48 hours. The chlorophyll loss in infected leaves by 96 hours was 44% compared with controls.

Subjecting inoculated leaves of intact plants to a controlled atmospheric-environmental system with an atmospheric pressure of 233 millibars and O₂ and CO₂ partial pressures adjusted to approximately that of normal ambient pressure during infection and disease development prevented most midvein chlorosis and complete chlorosis, but did not prevent necrotic lesion or chlorotic halo development. Under the hypobaric conditions, chlorophyll loss during disease development was reduced to 22% compared with controls at 96 hours. The observations suggest that ethylene may function late in pathogenesis of this host-pathogen interaction and is responsible for much of the chlorophyll loss after its maximum production at 48 hours.