Abstract: Creeping bentgrass seedlings cv. ‘Penn-A4’ infected with Rhizoctonia solani, which was produced by the induced-systemic-resistance (ISR) disease-resistance action induced by butanediol (BDO), was sprayed with different concentrations of the ethylene synthesis inhibitor, CoCl₂ and ethylene synthesis promoter, 1-amino cyclopropane carboxylic acid (ACC). Subsequently, changes inascorbic acid (AsA) and glutathione (GSH) contents and related enzyme activity in theascorbate-glutathione (AsA-GSH) cycle in seedlings were measured. Paraffin sectioning and fluorescence microscopy techniques were used to assess the effects of ethylene on callose deposition during ISR disease-resistance reactions. Under low ethylene concentrations AsA content was low and ascorbate peroxidase (APX) activity was reduced. A large amount of GSH was catalytically reduced to oxidize glutathione (GSSG) which accumulated. Glutathione reductase (GR) activity was low; GSSG is reduced to GSH by GR, consequently GSH remained at low levels. However, under high ethylene concentrations, AsA content was high and APX activity was higher. GSSG was catalytically reduced to GSH which accumulated. Therefore, in ISR disease-resistance reaction, high concentrations of ethylene induced the accumulation of AsA and GSH, which involved not only in the metabolic balance of reactive oxygen species, but also acted as signaling molecules playing an important role in the disease resistance of ISR. Callose was mainly deposited in sclerenchyma cells, phloem, xylem tissues and epidermis seedling leaves in ISR reaction induced by BDO. Callose deposition was highest in sclerenchyma cell and least in the epidermis. Callose deposition areas had differences in ethylene signal compounds but became less significant with reduced treatment time. Ethylene concentration affected callose deposition in ISR reaction induced by BDO; callose deposition increased significantly with reduced treatment time. Areas of callose deposition occupied 9.916 mm² under 100 μmol·L^-1 ACC treatment after 5 d, and increased to 38.396 mm² after 10 d. However, in the later stages of disease invasioncallose deposition area decreased to 20.052 mm² under 100 μmol·L^-1 ACC after 15 d. These results suggest that the ethylene molecular signalhas a short-term effect on callose deposition and increased the disease-resistance of creeping bentgrass. This research provides a theoretical basis for the exploration of ET signal molecules to control the physiological characteristics of resistance in ISR resistance response in creeping bentgrass.

Key words: creeping bentgrass (Agrostis stolonifera), AsA-GSH cycle, callose, ethylene, butanediol, ISR disease-resistance response, paraffin sectioning